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 radiology 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 accounts 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 asymptomatic 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 trachea 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: [email protected] 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.

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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 obstructions 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 present, 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: aspiration 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 attempted 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

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 immediately if the patient has an unstable airway, the patient should be taken to the operating 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 circumstances, 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 emergent airway problem. In most circumstances, definitive management of a compromised 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 secretions 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 instruments 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 situations are among the most stressful in all of medicine, because in most circumstances, 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

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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 bronchial, 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 ulceration. 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 diameter 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 intervention 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 treatment 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 factors for recurrent bleeding after IR embolization: residual mild bleeding beyond the first week after intervention, need for blood transfusion before the procedure, and aspergilloma 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 reports of successful medical treatment with oral and intravenous tranexamic acid in patients 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 hemoptysis 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 options 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

fistulas, iatrogenic pulmonary artery rupture, chest trauma, and recurrent lifethreatening 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 after 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 unstable 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 collapses. 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 fatigue. Patients with secondary SP are more likely to be symptomatic because of the underlying lung disease. Physical examination findings become prominent as the patient 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

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 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 typically 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 accomplished 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 patients, 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 guidance. The CT scans should be performed with the existing tubes on suction to evaluate for incomplete lung expansion. Definitive surgical treatment options consist of open thoracotomy versus videoassisted 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 performed. 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 accomplished 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 uncomfortable but seems to have a recurrence rate as high as 5%.20 Summary

Spontaneous pneumothorax can be either primary or secondary in nature. All symptomatic 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 associated 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

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 typically present with subtle symptoms, most commonly failure to thrive, with anorexia, weight loss, and poor energy. Symptoms, including fever, cough, tachypnea, desaturation, 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 findings 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

Fluid characteristics (1 of the following)

Early

Intermediate

Late

pH 2.5 g/dL White blood cell count >500/mL Specific gravity >1.018

Thick opaque fluid Positive culture

Organizing peel with entrapment of the lung

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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 thoracentesis 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 patients 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 infections 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 recommended. 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 treatment at our facility is typically 3 to 5 days of lytic therapy. After this treatment, repeat imaging 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 Intrapleural 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 therapy. 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 complex and multiloculated effusions, surgical intervention may be required. An attempt at chest tube drainage with the addition of intrapleural streptokinase may obviate surgical 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 lifethreatening 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.

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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 haemoptysis 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 longterm 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 streptokinase for pleural infection. N Engl J Med 2005;352:865–74.

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This article discusses thoracic emergencies, including the anatomy, pathophysiology, clinical presentation, examination, diagnosis, technique, managem...
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