Thoracic Emergencies

Stephanie G. Worrell, MD, Steven R. DeMeester, MD*

KEYWORDS
 Upper airway obstruction  Massive hemoptysis  Spontaneous pneumothorax
 Pulmonary empyema

KEY POINTS
 Rigid bronchoscopy can handle almost any cause of airway obstruction.
 The current first-line treatment of managing massive hemoptysis is interventional radi-
ology embolization after stabilization of the airway.
 The decision to surgically treat for prevention of recurrence depends on the cause and to
some extent the risk associated with recurrence.

ACUTE UPPER AIRWAY OBSTRUCTION

Introduction
The incidence of death from acute airway obstruction in adults increases with age and
peaks at 85 years old.1 The most common cause is aspiration of a foreign body. This
situation leads to sudden obstruction of an otherwise normal airway in most instances.
Other causes include trauma, inflammation, tumors, and neurologic diseases. Apart
from trauma, these other causes are usually chronic, but when they reach a critical
point, they present as acute airway obstruction. The most common cause of chronic
airway obstruction is tracheal stenosis related to prior intubation. This condition ac-
counts for approximately 90% of cases.2 Intubations as short as 24 hours can lead
to tracheal stenosis.3 Often, patients with chronic airway compromise are asymptom-
atic at rest but may note stridor or dyspnea on exertion.
Critical stenosis occurs when the diameter of the airway has decreased to 25% or
less of the normal tracheal diameter. The normal diameter varies for individuals and is
typically 15 to 25 mm. In general, critical stenosis occurs when the diameter of the tra-
chea is less than 4 mm (Fig. 1).

Anatomy/Pathophysiology
Upper airway obstruction is defined as an obstruction of the airway at any location
from the mouth to the carina. The narrowest portion of the upper airway is the larynx

Disclosures: None.
Department of Surgery, Keck School of Medicine, University of Southern California, 1510 San
Pablo Street, Suite 514, Los Angeles, CA 90033, USA
* Corresponding author.
E-mail address: steven.demeester@med.usc.edu

Surg Clin N Am 94 (2014) 183–191

http://dx.doi.org/10.1016/j.suc.2013.10.013 surgical.theclinics.com
0039-6109/14/$ – see front matter Ó 2014 Elsevier Inc. All rights reserved.
184 Worrell & DeMeester

Fig. 1. Tracheal mass semiobstructing the airway before and after removal by coring out the
mass.

at the glottis in adults and the subglottic region in infants. Most foreign body obstruc-
tions occur in this area. However, obstruction can occur at any location in the upper
airway.
Clinical Presentation/Examination

Presenting signs and symptoms

Cough
Hoarseness
Shortness of breath
Dyspnea on exertion
Stridor (biphasic if within the extrathoracic trachea)
Use of accessory muscles
Nasal flaring
Chest wall retractions
Cyanosis
Decreased consciousness

Diagnosis
Rapid diagnosis and treatment are critical to patient survival. Complete upper airway
obstruction can lead to cardiac arrest and death within minutes. Once stridor is pre-
sent, the airway is already severely compromised. It is imperative to first assess the
degree of obstruction. This situation can quickly be evaluated by the distress of the
patient. Are they working hard to breathe? Can they talk?
The cause of upper airway obstruction can be broken down into 2 categories: aspi-
ration versus nonaspiration. With aspiration, there is typically a clear history of the
event. No endotracheal tube should be placed to avoid potentially pushing the object
more distally in to the oropharynx. Instead, the Heimlich maneuver should be attemp-
ted if feasible. If this maneuver is not successful or feasible and the patient is stable
and moving air, the safest option is to rapidly bring the patient to the operating
 Thoracic Emergencies 185

room for a rigid bronchoscopy. If the patient has no airway or an inadequate airway, an
immediate cricothyrotomy should be performed.
The second cause is nonaspiration, typically a stricture or tumor. If the patient is
able to maintain a patent airway and time permits, a computed tomography (CT)
scan should be obtained to define the level of obstruction. Again, no intubation should
be attempted, because this may exacerbate the problem. After the CT scan, or imme-
diately if the patient has an unstable airway, the patient should be taken to the oper-
ating room. While awaiting the operating room, heliox, a gaseous mixture of helium
and oxygen, can be given to the patient. Heliox can temporize the airway and
decrease the work of breathing before intervention. Initially, a flexible bronchoscopy
can be performed, with minimal sedation if the patient is stable. This procedure allows
an assessment of the cause and location of the obstruction. However, in most circum-
stances, the bronchoscope should not be advanced through the lesion, because even
a small amount of blood or inflammation can convert a marginal airway into an emer-
gent airway problem. In most circumstances, definitive management of a compro-
mised airway is best performed with a rigid bronchoscope. These scopes allow
coring out of an airway tumor and dilatation of a stricture, along with removal of secre-
tions and any aspirated material. In some circumstances, balloon dilatation through a
flexible bronchoscope is reasonable, but a rigid bronchoscope should be immediately
available in case the balloon dilatation is unsuccessful or induces bleeding. Before
beginning the procedure, it is imperative that everything is laid out so that all instru-
ments are immediately accessible. The guiding principle is that once the procedure
has begun, there is no time to find additional pieces of equipment or replacements
without compromising the ability to save the patient. The light source should be
attached to the rigid and the flexible bronchoscope and tested. In addition, a backup
light source should be in the room. Useful adjuvant equipment includes the argon
beam for hemostasis or further debridement of a tumor or stricture, and dilute
epinephrine irrigation for hemostasis.
Once everything is assembled, a decision is made based on the status of the airway
to initially evaluate with the flexible bronchoscope or to go in immediately with the rigid
bronchoscope. When going in with a rigid bronchoscope, I prefer to rapidly paralyze
the patient to avoid bucking and coughing, which can complicate an already high-risk
procedure. However, once the patient is paralyzed, it is unlikely that mask respiration
will be successful in someone with a compromised airway, so familiarity with rigid
bronchoscopy is essential. Even when practitioners are very experienced, these situ-
ations are among the most stressful in all of medicine, because in most circum-
stances, there is little more than 2 minutes to establish an adequate airway.

Summary
Establishing an airway is the most critical component to treating a patient with upper
airway obstruction. This is one of the most challenging and stressful situations in all of
medicine. Often, there is only 2 to 3 minutes to save a patient’s life and familiarity with
rigid bronchoscopy is essential. Rigid bronchoscopy can handle almost any cause of
airway obstruction.

MASSIVE HEMOPTYSIS
Introduction
Massive hemoptysis is usually defined as coughing up 600 mL or more of blood within
24 hours.4 Mortality associated with massive hemoptysis ranges from 5% to 15%,
mainly related to asphyxiation, as the airway fills with blood.5–8 The main causes
186 Worrell & DeMeester

underlying massive hemoptysis include bronchiectasis, tuberculosis, mycetomas,

necrotizing pneumonia, and bronchogenic carcinomas.9 Patients with cystic fibrosis
are also presenting at increasing rate and are at an increased risk of massive
hemoptysis.10
The feeder vessels typically associated with massive hemoptysis include the bron-
chial, intercostal, and accessory arteries off the subclavian artery. Among the common
causes (bronchiectasis, tuberculosis, and infection) the cause of bleeding is usually
inflammation of the airway, with rupture of the bronchial arteries from dilation or ulcer-
ation. Rarely, the pulmonary artery can be associated with massive hemoptysis, as
seen in Rasmussen aneurysm.

Clinical Presentation/Examination
Massive hemoptysis can be life threatening. The first steps when a patient presents
are to establish a patent airway and volume resuscitate as necessary. After this stage,
the most important step is to identify which lung is involved, right versus left, and then
to establish which lobe is involved. To evaluate this situation, a chest radiograph and
flexible bronchoscopy should be performed. A CT scan may be helpful to localize
bleeding, but in general, angiography is preferred. Angiography is preferred because
it can identify the source of bleeding and then treat with embolization in the same
setting. Angiography has recently become the preferred first-line treatment. In patients
with near airway obstruction from clotted blood, a rigid bronchoscopy may also be
necessary. However, most patients can be managed with a flexible bronchoscope
down a large endotracheal tube for suctioning of blood.
In general, intubation with a double lumen tube is avoided, because the small diam-
eter of each lumen makes suctioning of the airway difficult. In cases of truly massive
and continued hemoptysis, in which the side or lobe is known, a bronchial blocker or
double lumen tube may temporize the situation until embolization or operative inter-
vention is performed.

Technique
The airway should be suctioned with a bronchoscope to obtain a patent airway.
Lavage with cold saline or vasoactive agents can be attempted; however, this is not
so effective for massive hemoptysis. These techniques are more useful when used
for postbiopsy-induced hemorrhage. This situation is in part because the agent is
washed away by the brisk bleeding.11 After stabilization of the airway, definitive treat-
ment of the feeder vessel is required.
Interventional radiology (IR) with embolization is currently first-line therapy. There is
a reported 10% to 29% recurrence rate, likely because of incomplete embolization,
recanalization, or collateral circulation.9 The following have been identified as risk fac-
tors for recurrent bleeding after IR embolization: residual mild bleeding beyond the first
week after intervention, need for blood transfusion before the procedure, and asper-
gilloma as the cause for bleeding.12 In these cases, IR embolization can be used as a
temporizing measure while waiting for definitive surgical resection. There are some re-
ports of successful medical treatment with oral and intravenous tranexamic acid in pa-
tients with cystic fibrosis who have failed multiple IR embolizations.13 Failure of IR
embolization may also indicate that the bronchial artery is not the source of the he-
moptysis and that an additional feeder artery that has not been embolized may be
the source. Repeated efforts to localize and embolize the source are reasonable op-
tions in a stable patient.
Surgery is being used less frequently, because of the high associated morbidity and
mortality. Surgery remains the best option for patients with complex arteriovenous
 Thoracic Emergencies 187

fistulas, iatrogenic pulmonary artery rupture, chest trauma, and recurrent life-
threatening hemoptysis.14 However, surgery is an option only if the source of bleeding
has been localized to a side or lobe. With the addition of multimodality therapies, the
morbidity and mortality associated with massive hemoptysis have dramatically
improved.4

Summary
The current first-line treatment of managing massive hemoptysis is IR embolization af-
ter stabilization of the airway. It is important to localize the side and if possible the lobe
that are the source of bleeding, with bronchoscopy and a chest radiograph. Surgical
resection is reserved for bleeding that does not respond to embolization or in an un-
stable patient with ongoing massive hemoptysis in whom the lobe involved has been
determined. The mortality with surgical resection, even in an elective setting, is high,
particularly with upper lobe sources secondary to the dense inflammation usually
associated with the underlying abnormality. Before any consideration of surgery, the
side and preferably the lobe involved with the bleeding must be known. Once both
lungs are filled with blood, it becomes difficult to identify the source, emphasizing
the importance of early bronchoscopy to localize the side of bleeding.

SPONTANEOUS PNEUMOTHORAX
Introduction
Spontaneous pneumothorax (SP) is defined as air in the pleural space, which can
occur as a primary or secondary cause. Primary SP occurs in patients with no known
underlying lung disease. In these patients, a CT scan is not necessary. These patients
are typically tall, thin men with low body mass index.15–17 Secondary SP is associated
with an underlying lung pathology, most commonly chronic obstructive pulmonary
disease, cystic fibrosis, tuberculosis, and lung cancer. In these patients, a CT scan
is useful to evaluate the underlying lung parenchyma.

Relevant Anatomy/Pathophysiology
A pneumothorax occurs when air collects between the visceral and parietal pleura. Air
usually enters the pleural cavity though a ruptured bleb in the lung during inspiration
and acts like a valve mechanism, allowing air to enter the pleural cavity, which cannot
escape. Corresponding to the increase in pleural pressure, the ipsilateral lung col-
lapses. This situation can progress to a tension pneumothorax if increased pressures
cause the mediastinum to shift and impair the ventilatory capacity of the contralateral
lung and the venous return to the heart.

Clinical Presentation/Examination
The most common presenting symptoms in a patient with pneumothorax are chest
pain and shortness of breath. The pain is often pleuritic and radiates to the ipsilateral
shoulder. Patients may also present with vague symptoms of anxiety, cough, and fa-
tigue. Patients with secondary SP are more likely to be symptomatic because of the
underlying lung disease. Physical examination findings become prominent as the pa-
tient develops tension physiology. Typical signs seen in a patient with a pneumothorax
include the following:
 Distant or absent breath sounds
 Tachypnea
 Asymmetric chest expansion
 Use of accessory muscles
188 Worrell & DeMeester

 Tachycardia
 Hypotension
 Jugular venous distention

Diagnostic Procedures/Treatment
Management depends on a primary versus secondary cause. In primary SP, after the
initial event, patients are at an approximately 30% risk of experiencing a recurrent
episode.18 Most commonly, patients are not offered surgical intervention for the first
event, but a second event warrants treatment. In patients at high risk for problems
related to a pneumothorax, such as airline pilots and scuba divers, intervention is typi-
cally offered with the first event.
Regardless of the cause, the treatment of a symptomatic patient involves drainage
of the pleural space and reexpansion of the lung. In an asymptomatic patient with a
small pneumothorax, simple observation is acceptable. Drainage can be accom-
plished by aspiration with an intravenous or thoracentesis catheter; however, success
rates are often low.19 Placement of a traditional chest tube or pigtail catheter is the
treatment of choice for an unstable or significantly symptomatic patient. In most pa-
tients, the air leak seals once the lung is fully reexpanded, but a prolonged leak beyond
7 days is an indication for surgical intervention, provided the lung is fully inflated with
the aid of additional chest tubes or pigtail catheters as necessary, often with CT guid-
ance. The CT scans should be performed with the existing tubes on suction to eval-
uate for incomplete lung expansion.
Definitive surgical treatment options consist of open thoracotomy versus video-
assisted thoracic surgery (VATS) technique. A transaxillary thoracotomy provides
excellent exposure, and the incision is hidden in the axilla. In patients with primary
pneumothorax, the source is almost always small blebs at the apex of the upper
lobe or on the superior segment of the lower lobe. If blebs are present, they should
be excised. After excision of any disease, an effective pleurodesis needs to be per-
formed. This procedure is key, because the underlying goal is to prevent the lung
from collapsing when new blebs occur in the future. This goal is more readily accom-
plished with the open technique, which has led to lower recurrence rates with an open
versus VATS approach. The gold standard approach with a rate of recurrence of less
than 1% is an open approach with resection of blebs and pleurectomy/pleurodesis.15
However, this rate of recurrence must be weighed against the increased patient
discomfort associated with this procedure. A VATS approach may be less uncomfort-
able but seems to have a recurrence rate as high as 5%.20

Summary
Spontaneous pneumothorax can be either primary or secondary in nature. All symp-
tomatic patients should be managed with drainage. The decision to surgically treat
for prevention of recurrence depends on the cause and, to some extent, the risk asso-
ciated with recurrence. VATS is a less morbid procedure; however, it has an increased
risk of failure.

PULMONARY EMPYEMA
Introduction
Pulmonary empyema is the collection of suppurative fluid in the pleural space (Fig. 2).
This condition can be from a thoracic injury, secondary to an underlying pneumonia, or
a parapneumonic effusion. The American Thoracic Society breaks an empyema down
in to 3 stages: early exudative, intermediate fibrinopurulent, and late organizing.21
 Thoracic Emergencies 189

Fig. 2. Empyema with air fluid level.

Historically, drainage of an empyema was performed with an open technique, with an

associated 70% mortality.22 The advent of closed tube drainage significantly
improved this mortality.

Clinical Presentation/Examination
A high index of suspicion is needed to make the diagnosis of empyema. Patients typi-
cally present with subtle symptoms, most commonly failure to thrive, with anorexia,
weight loss, and poor energy. Symptoms, including fever, cough, tachypnea, desatu-
ration, and leukocytosis are usually associated with the underlying cause, such as
pneumonia, and are not always present. A common cause of empyema is infection
of a pleural effusion in the setting of pneumonia.

Diagnosis
When a chest radiograph or CT scan shows a pleural fluid collection, fluid sampling
and analysis are the first steps in deciding the appropriate treatment. If the effusion
is loculated, air fluid levels may be apparent on plain film. The diagnosis of empyema
is based on the composition of the fluid and the radiographic characteristics. The fluid
has different characteristics based on the stage of the empyema (Table 1). These find-
ings are determined by imaging and examination of the fluid. Although an organizing
peel defines the late stage, CT and ultrasonography are not uniformly predictive for
diagnosis.

Table 1
Stages of pulmonary empyema

Early Intermediate Late

Fluid characteristics pH <7.2 Thick opaque Organizing peel
(1 of the following) Glucose <40 mg/dL fluid with entrapment
Lactate dehydrogenase Positive culture of the lung
>1000 IU/dL
Protein >2.5 g/dL
White blood cell count
>500/mL
Specific gravity >1.018
190 Worrell & DeMeester

Management
Once the diagnosis of empyema has been made, attention to removal of the purulent
fluid and reexpansion of the lung are critical. If an empyema is in the early stage, a thor-
acentesis and antibiotics may be adequate treatment. The antibiotics are not initiated
for treatment of the empyema but for treatment of the underlying pneumonia. In the
absence of an underlying pneumonia, no antibiotics should be used, because they
cannot enter the pleural space and therefore offer no benefit to the patient. For pa-
tients with an underlying pneumonia, empirical antibiotics should be started while
awaiting culture results of the fluid based on the common causes of infection. For
community-acquired pneumonia with empyema, streptococcal and anaerobic infec-
tions are most common and multidrug-resistant Staphylococcus is most commonly
found in hospital-acquired pneumonia with empyema.23
For larger single homogeneous fluid collections, drainage with a chest tube is recom-
mended. The size of the chest tube was initially believed to be important. However,
recent studies have shown that smaller-bore chest tubes have similar outcomes to
larger chest tubes. After drainage, a CT scan should be obtained to look for residual fluid.
Streptokinase or another form of lytic therapy can be used to decrease the need for
operative intervention; however, the data on outcomes are mixed.24 The first-line treat-
ment at our facility is typically 3 to 5 days of lytic therapy. After this treatment, repeat im-
aging should be obtained. If progress is being made, then lytic treatment should be
continued. If there is no progress after 5 days, then an alternative treatment plan should
be made.
The role of surgery in empyema may be declining. In the MIST1 (Multicenter Intra-
pleural Sepsis 1) trial,25 only 18% of patients failed treatment with antibiotics and
chest tube drainage and required operation. Patients may require VATS if there is
incomplete drainage despite adequate chest tube placement and streptokinase ther-
apy. However, in the presence of a thick peel, an open approach may be necessary.
For a persistent cavity, treatment to obliterate the space is required. The options are
decortication, an Eloesser flap, thoracoplasty, or filling in the space with muscle.
Determination of which approach to use depends on patient age, comorbidities, the
size of the cavity, and the underlying condition of the lung.

Summary
Initial treatment of pulmonary empyema requires drainage and antibiotics. With com-
plex and multiloculated effusions, surgical intervention may be required. An attempt at
chest tube drainage with the addition of intrapleural streptokinase may obviate surgi-
cal intervention; however, results are mixed.

REFERENCES

1. Choking. Available at: http://www.nsc.org/safety_home/HomeandRecreational

Safety/Pages/Choking.aspx#older%20adults. Accessed June 20, 2013.
2. McCaffrey TV. Classification of laryngotracheal stenosis. Laryngoscope 1992;
102:1335–40.
3. Yang K. Tracheal stenosis after a brief intubation. Anesth Analg 1995;80:625–7.
4. Shigemura N, Wan IY, Yu SC, et al. Multidisciplinary management of life-
threatening massive hemoptysis: a 10-year experience. Ann Thorac Surg 2009;
87(3):849–53.
5. Dweik RA, Stoller JK. Role of bronchoscopy in massive hemoptysis. Clin Chest
Med 1999;20(1):89–105.
 Thoracic Emergencies 191

6. Corey R, Hla KM. Major and massive hemoptysis: reassessment of conservative

management. Am J Med Sci 1987;294(5):301–9.
7. Crocco JA, Rooney JJ, Tankushen DS, et al. Massive hemoptysis. Arch Intern
Med 1968;121(6):495–8.
8. Hirshberg B, Biran I, Glazer M, et al. Hemoptysis: etiology, evaluation, and
outcome in a tertiary referral hospital. Chest 1997;112(2):440–4.
9. Sakr L, Dutau H. Massive hemoptysis: an update on the role of bronchoscopy in
diagnosis and management. Respiration 2010;80:38–58.
10. Flume PA, Yankaskas JR, Ebeling M, et al. Massive hemoptysis in cystic fibrosis.
Chest 2005;128(2):729–38.
11. Cahill BC, Ingbar DH. Massive hemoptysis, assessment and management. Clin
Chest Med 1994;15:147–67.
12. Van den Heuvel MM, Els A, Koegelenberg CF. Risk factors for recurrence of hae-
moptysis following bronchial artery embolization for life-threatening haemoptysis.
Int J Tuberc Lung Dis 2007;11:909–14.
13. Wong LT, Lillquist YP, Culham G, et al. Treatment of recurrent hemoptysis in a
child with cystic fibrosis by repeated bronchial artery embolizations and long-
term tranexamic acid. Pediatr Pulmonol 1996;22:275–9.
14. Jean-Baptise E. Clinical assessment and management of massive hemoptysis.
Crit Care Med 2000;28:1642–7.
15. MacDuff A, Arnold A, Harvey J. Management of spontaneous pneumothorax: British
Thoracic Society Pleural Disease Guideline 2010. Thorax 2010;65(Suppl 2):ii18–31.
16. Bense L, Eklund G, Wiman LG. Smoking and the increased risk of contracting
spontaneous pneumothorax. Chest 1987;92:1009–12.
17. Grundy S, Bentley A, Tschopp JM. Primary spontaneous pneumothorax: a diffuse
disease of the pleura. Respiration 2012;83:185–9.
18. Gobbel W. Spontaneous pneumothorax. J Thorac Cardiovasc Surg 1963;46:
331–45.
19. Baumann MH, Strange C. Treatment of spontaneous pneumothorax: a more
aggressive approach? Chest 1997;112:789–804.
20. Hatz RA, Kaps MF, Meimarakis G, et al. Long-term results after video-assisted
thoracoscopic surgery for first-time and recurrent spontaneous pneumothorax.
Ann Thorac Surg 2000;70:253–7.
21. Andrews NC, Parker EF, Shaw RP, et al. Management of nontuberculous
empyema. Am Rev Respir Dis 1962;85:935–6.
22. Peters RM. Empyema thoracis: historical perspective. Ann Thorac Surg 1989;48:
306–8.
23. Maskell NA, Batt S, Hedley EL, et al. The bacteriology of pleural infection by
genetic and standard methods and its mortality significance. Am J Respir Crit
Care Med 2006;174:817–23.
24. Cameron R, Davies HR. Intra-pleural fibrinolytic therapy versus conservative
management in the treatment of adult parapneumonic effusions and empyema.
Cochrane Database Syst Rev 2008;(2):CD002312.
25. Maskell NA, Davies CW, Nunn AJ, et al. Controlled trial of intrapleural streptoki-
nase for pleural infection. N Engl J Med 2005;352:865–74.