Pneumothorax and Barotrauma

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Pneumothorax and Barotrauma

Robert C. Hyzy and Rommel Sagana

Chapter Outline

Definition and History

Pneumothorax is defined as air in the pleural space because of a break in the visceral or parietal pleura. The term pneumothorax was used for the first time in 1803.¹ Laennec² gave the first clinical description of pneumothorax in 1819; however, the first chest radiograph demonstrating this entity was not published until 1901.³ Definitive therapy became available with the advent of tube thoracostomy in 1876.⁴ It was thought to be always associated with tuberculosis until 1932 when “spontaneous pneumothorax in the apparently healthy” was first described.⁵

Spontaneous pneumothorax can be classified as primary or secondary. Primary spontaneous pneumothorax (PSP) occurs in patients with no apparent underlying lung disease. Secondary spontaneous pneumothorax (SSP) occurs in association with a known underlying lung disease such as chronic obstructive pulmonary disease (COPD).⁶ Nonspontaneous causes of pneumothorax include traumatic and iatrogenic (Table 47.1).

Table 47.1

Classification of Pneumothorax

From Grundy S, Bentley A, Tschopp JM: Primary spontaneous pneumothorax: A diffuse disease of the pleura. Respiration 2012;83:185-189.

Incidence

The incidence of PSP in men varies geographically, from 7.4 per 100,000 population per year in the United States to 37 per 100,000 population per year in the United Kingdom. In women, the incidence is substantially less, ranging from 1.2 per 100,000 population per year in the United States to 15.4 per 100,000 population per year in the United Kingdom.⁷ The reason for these differences is not known. In a study that evaluated 1199 patients with pneumothorax that included 865 male patients and 334 female patients, 60.3% of the pneumothoraces were spontaneous, 33.6% were traumatic, and 6.1% were iatrogenic.⁸

The estimates of the incidence of recurrent PSP range from 20% to more than 50% with most recurrences occurring within the first year.⁹

Pathophysiology

Emphysema-like Changes

PSP occurs in patients with no previously known lung disease. It is important to note, however, that this does not mean there is no underlying pathologic process. A finding of abnormal pleura is very common in PSP if looked for carefully.¹⁰ Abnormalities seen in PSP are summarized in Table 47.2 and include blebs and bullae, which are otherwise known as emphysema-like changes (ELCs). These areas of weakness of the visceral pleura are prone to rupture, allowing air to leak into the pleural space. Abnormalities can be visualized radiographically with high-resolution computed tomography (CT) scans and macroscopically at thoracoscopy.^10,11 High-resolution CT imaging reveals these defects in approximately 80% of PSP patients. The literature is mixed as to whether the presence of or extent of ELCs is directly related to the risk of recurrence. Some case series suggest that there is no association,^12,13 although others suggest the presence of contralateral blebs/bullae is a risk factor for future pneumothorax.^14,15 The only clear conclusion that can be drawn is that there is a direct association between the presence of ELCs and the occurrence (but not necessarily recurrence) of a pneumothorax (Table 47.2 and Fig. 47.1).

Table 47.2

Pathologic Changes Associated with Primary Spontaneous Pneumothorax (PSP)

From Grundy S, Bentley A, Tschopp JM: Primary spontaneous pneumothorax: A diffuse disease of the pleura. Respiration 2012;83:185-189.

Figure 47.1 Large bulla at the apex of the left lung in a 12-year-old boy with recurrent primary spontaneous pneumothorax. (From Noppen M, De Keukelieire T: Pneumothorax. Respiration 2008;76:121-127.)

Pleural Porosity

ELCs are not the sole cause of PSP. Air leak has been described in areas where no ELCs are seen, leading to the concept known as “pleural porosity.”16,17 When evaluated with fluorescein-enhanced autofluorescence, areas of high-grade abnormality in the visceral pleura were frequently visualized separate from any area of abnormality seen with white light at thoracoscopy in patients with PSP. High-grade abnormalities were not seen in control patients.¹⁸ Areas of fluorescein leak (i.e., areas of potential air leak) were visualized in only a small proportion of PSP, but these areas were noted to be distinct from areas of ELC. When studied with electron microscopy, the linings of some resected areas of ELC have been shown to be almost completely absent of mesothelial cells and have abnormal pores present¹⁹ (Fig. 47.2).

Figure 47.2 Air leak identified by fluorescein-enhanced autofluorescence thoracoscopy in a 27-year-old man with recurrent primary spontaneous pneumothorax. The air leak was situated at the base of a highly vascularized, severe malformation of the apex of the lung. (From Noppen M, De Keukelieire T: Pneumothorax. Respiration 2008;76:121-127.)

Distal Airway Inflammation

Pathologic findings suggest an inflammatory cause to the formation of ELCs. Chronic distal airway inflammation with lymphocyte and macrophage infiltration alongside fibrotic changes and compensatory emphysema can be seen microscopically in areas of lung tissue from patients with PSP.²⁰ In a different study, the presence of respiratory bronchiolitis (RB) was seen in close to 90% of patients with PSP who underwent surgical resection in a different study.²¹ However, all these patients in this study were smokers, and smoking is a recognized cause of RB. It has been proposed that distal airway inflammation associated with PSP leads to obstructive gas trapping and consequent increases in distal airway pressure, which possibly causes air leak into the pleural space.²²

Smoking

Cigarette smoking is a significant risk factor for PSP. It is thought to be due to the consequences of airway inflammation leading to airway obstruction with a check valve phenomenon, causing air trapping and development of pneumothorax.²² The lifetime risk is 12% in smokers compared to 0.1% in nonsmokers. Risk is also directly related to the amount of cigarette smoking. Compared to nonsmokers, the relative risk of PSP in men was seven times higher in light smokers (1-12 cigarettes per day), 21 times higher in moderate smokers (13-22 cigarettes per day), and 102 times higher in heavy smokers (>22 cigarettes per day). For women, the relative risk was 4, 14, and 68 times higher in light, moderate, and heavy smokers, respectively.²³ Cessation of smoking appears to reduce the risk of recurrence,⁹ and continued smoking increases the risk of recurrence.²⁴

RB, a form of airway inflammation associated with cigarette smoking, may contribute to the development and recurrence of PSP. In a study with 115 patients with PSP who underwent video-assisted thoracoscopic surgery (VATS), pneumothorax recurrence rates were higher in patients with extensive rather than nonextensive RB for both nonoperative and postoperative pneumothorax.²⁵

Genetics

Familial inheritance of pneumothorax describing the clustering of PSP in certain families has been published. Autosomal dominant, autosomal recessive, polygenic, and X-linked recessive inheritance mechanisms have been proposed.26–28 Birt-Hogg-Dubé (BHD) is an autosomal dominant cancer disorder that predisposes patients to benign skin tumors and renal cancer. It is associated with pleuropulmonary blebs and cysts that lead to PSP.²⁹ In one study of 198 patients with this syndrome, 48 patients (24%) had a history of pneumothorax.³⁰ The gene responsible for this familial cancer syndrome (FLCN) has been mapped to chromosome 17p11.2.^31,32 Other mutations of FLCN have been associated with spontaneous pneumothorax and bullous lung disease in the absence of Birt-Hogg-Dubé syndrome.³³

Patients with Marfan syndrome are tall, and pneumothorax is a common pulmonary complication. Marfan syndrome is caused by the mutation in FBN1 gene on chromosome 15. This gene is responsible for the formation of 10- to 12-nm microfibrils in the extracellular matrix of connective tissue. It is hypothesized that familial spontaneous pneumothorax is caused by a connective tissue disorder that exhibits mendelian inheritance and FBN1 has been postulated as the causative gene.³⁴

Classification

Spontaneous Pneumothorax

Primary Spontaneous Pneumothorax

PSP is classically seen in previously healthy young men with an asthenic body habitus. The incidence of PSP rises with increasing height among adults of both sexes, more so in men. For those 76 inches or taller, the rate was 200 per 100,000 person-years.³⁵ It is hypothesized that individuals with tall stature and low body mass index combined with smoking are predisposed to develop ELCs owing to the pressure gradient between the lung base and the apex, resulting in increased alveolar distending pressures at the apex.³⁶ Smoking, as previously described, greatly increases the risk of PSP. Smoking increases the relative risk of developing spontaneous pneumothorax about ninefold in women and 22-fold in men, and there is a statistically significant dose-response relationship between smoking and spontaneous pneumothorax.³⁷

Secondary Spontaneous Pneumothorax

SSP has been described in a large variety of diseases including COPD with emphysema, cystic fibrosis (CF), tuberculosis, lung cancer, human immunodeficiency virus (HIV)-associated Pneumocystis jiroveci pneumonia, followed by more rare but “typical” disorders such as lymphangioleiomyomatosis (LAM) and histiocytosis X (Box 47.1). Because lung function in these patients is already compromised, SSP often presents as a potentially life-threatening disease requiring immediate action, as opposed to PSP, which is more of a nuisance than a dangerous condition. The general incidence is almost similar to that of PSP.³⁸

Chronic Obstructive Pulmonary Disease

COPD is the most common cause of SSP, with nearly 70% of SSP attributed to COPD.³⁹ The peak incidence of SSP from COPD typically occurs later in life averaging 60 to 65 years of age.⁴⁰ The clinical presentation of pneumothorax in COPD is often atypical—pain may be absent, anxiety and breathlessness may predominate and be out of proportion to the collapsed lung, and the classic sign of hyperresonance may not be helpful because of the underlying emphysema. The air leak in these patients is usually large, and the tissues are slow to heal, so it is weeks before the tubes can be taken out.⁴¹

Pneumothorax in Drug Abusers

When the peripheral veins of chronic abusers of drugs become obliterated because of a sclerotic or infectious process, the individual may attempt to use larger veins in the groin or neck. Attempted subclavian or supraclavicular (“pocket shot”) injection of drugs in the street setting has led to unilateral or bilateral pneumothoraces.42–44 Douglas and Levison⁴⁵ found that the incidence of pneumothoraces is equal in both sexes and that it is less of a problem in teenagers and in addicts older than 40 years of age. It was also noted that although most drug users describe using small (21- or 22-gauge) needles, a large, complete, or tension pneumothorax usually develops.

Pneumothorax in HIV-Infected Patients

Pneumothorax is an uncommon but potentially fatal complication of HIV infection. The first report of spontaneous pneumothorax in patients with acquired immunodeficiency syndrome (AIDS) was in 1984.⁴⁶ With the diagnosis of AIDS, a patient’s risk of sustaining a nontraumatic pneumothorax increases to 450 times that of the general population.⁴⁷ It has since been described in a generalized HIV-infected population.^48,49 Pneumothorax complicated 1.2% of all hospital admissions in a cohort of 599 HIV-infected patients followed over 3 years in a prospective observational study. There was also an associated increase in in-hospital mortality rate (31% versus 6%) for patients without pneumothorax.⁴⁸

A high incidence (2-9%) of pneumothorax has been reported in patients with AIDS and Pneumocystis carinii pneumonia (PCP).50–52 Pneumocystis carinii, which was thought to be a protozoan, has been renamed as Pneumocystis jiroveci and is now classified as an archiascomycetous fungus.⁵³ Causes of pneumothorax in HIV-infected individuals include P. jiroveci^54–57 along with other infectious agents such as Mycobacterium tuberculosis, M. avium intracellulare, pulmonary cytomegalovirus, Pneumococcus organisms,⁵⁴ or pulmonary toxoplasmosis.⁵⁴ Pneumothorax has also been described in HIV-infected individuals from Kaposi sarcoma.⁵⁸

The cause of pneumothorax in patients with PCP is unclear. Several investigators believe that extensive tissue invasion within the alveolar interstitium in severe PCP is an important factor in causing necrosis and subsequent pneumothorax. Several observations highlight this point. The most common sites of tissue invasion with PCP are the alveolar septa, pleurae, and vasculature.⁵⁹ Tissue invasion could cause necrosis as a result of direct tissue injury by toxins from Pneumocystis,⁵⁹ infarction from vascular compromise,^60,61 or as a result of the host inflammatory response.⁶²

The administration of aerosolized pentamidine has been implicated in the pathogenesis of cavitation, cyst formation, and pneumothorax,50,63,64 but the biologic basis for this relationship is unknown. No direct toxic action of pentamidine on the lungs has been described, so an indirect effect may be present. Cavitation due to PCP may occur primarily in the upper lobes and periphery because aerosolized pentamidine is preferentially delivered to the proximal parenchyma of the lower lobes. Inadequate deposition of pentamidine in the periphery of the lung could allow a chronic, low-grade infection with Pneumocystis to persist, leading to peripheral lung destruction and pneumatocele formation. Increased survival time of AIDS patients due to prophylaxis could allow for development of these lesions.⁵⁰

Several other risk factors for AIDS-related pneumothorax have been identified. In addition to previous or active infection of P. jiroveci and aerosolized pentamidine, cigarette smoking and the presence of pneumatoceles on chest radiograph are risk factors.⁶⁵ The association between cigarette smoking and AIDS-related pneumothorax could be explained by subclinical obstructive disease preventing adequate deposition of aerosolized pentamidine in the lung periphery, resulting in subpleural Pneumocystis infection.⁶⁵ Pulmonary tuberculosis also appears to increase the risk of pneumothorax in AIDS.⁶⁶

Catamenial Pneumothorax

In most cases, catamenial pneumothorax is related to pelvic or thoracic endometriosis.67,68 Catamenial pneumothorax occurs typically within 24 to 72 hours after onset of menstruation. It is often recurrent and more common than previously thought. Two mechanisms have been described for pneumothorax related to endometriosis. The most common is the movement of endometrial implants to the diaphragm, preferentially to the right side because of the recognized peritoneal circulation up from the pelvis to the right side. These implants then create channels or “holes” through the diaphragm that allow the implants or air to move into the chest. The second and much less frequent cause of endometrial implants causing pneumothorax in the chest is through the venous implants that lodge into the lung itself.⁶⁹ Clinical manifestations of thoracic endometriosis include chest pain, dyspnea, and hemoptysis. Treatment for the prevention of recurrence is indicated after a first episode of catamenial pneumothorax because recurrences are frequent.³⁸

Cystic Fibrosis

SSP occurs in approximately 6% of all patients with CF and this number increases to 16% to 20% among those who survive to age 18.70,71 SSP from CF is usually due to rupture of apical subpleural cysts. The risk of pneumothorax is inversely proportional to the forced expiratory volume in 1 second (FEV₁). Other factors associated with an increased risk of pneumothorax include infection with Pseudomonas aeruginosa, Burkholderia cepacia complex, or Aspergillus species. A previous history of massive hemoptysis also increases risk.

Nonspontaneous Pneumothorax

Traumatic Pneumothorax

Pneumothorax ranks second to rib fractures as the most common sign of chest trauma. It occurs in up to 50% of chest trauma victims.⁷² Most are caused by a penetrating injury, but closed chest trauma causing alveolar rupture from thoracic compression, fracture of a bronchus, and esophageal rupture have also been reported.^73,74 Traumatic pneumothorax can be classified as open, closed, tension, or hemopneumothorax. A tension pneumothorax should be managed immediately by decompression with a large-bore needle usually in the second anterior interspace in the midclavicular line. Open pneumothorax should have a moist sterile gauze pack placed over the open wound, followed by a chest tube. Hemopneumothorax (20% of trauma patients) requires insertion of a large-bore (28-36F) chest tube.³⁸

Occult pneumothorax may be present in half of blunt abdominal trauma patients, many of which are undetected by chest radiograph.75–79 CT of the chest should therefore always be performed in these patients. Most surgeons and emergency physicians will place a chest tube in occult and nonoccult pneumothoraces. Studies suggest, however, that clinically stable patients and those who do not have an enlarging pneumothorax may be treated conservatively, ultimately requiring chest tube placement in about 10% of cases.⁸⁰

Traumatic Iatrogenic Pneumothorax

Iatrogenic pneumothorax occurs most often following transthoracic needle biopsy (24%), subclavian vein catheterization (22%), thoracentesis (20%), transbronchial lung biopsy (10%), pleural biopsy (8%), and positive-pressure ventilation (7%).⁸¹ Diagnosis of iatrogenic pneumothorax is often delayed. Small and asymptomatic iatrogenic pneumothorax, however, often do not need any treatment and resolve spontaneously. In larger or symptomatic pneumothoraces, simple manual aspiration or placement of a small catheter or chest tube attached to a Heimlich valve is usually sufficient.⁸² Larger tubes may be necessary in patients with emphysema or when the patient is placed on a mechanical ventilator.

Pulmonary Barotrauma During Mechanical Ventilation

Pulmonary barotrauma (PBT) refers to alveolar rupture due to elevated transalveolar pressure (the alveolar pressure minus the pressure in the adjacent interstitial space). PBT was previously estimated to range between 3.8% and 41.7% of patients undergoing mechanical ventilation.⁸³ The rate in actuality may be lower because low tidal volume ventilation is becoming more common. Consequences of barotrauma include pneumothorax, pneumomediastinum, pneumoperitoneum, and subcutaneous emphysema.

Positive-pressure ventilation increases transalveolar pressure, which can cause alveolar rupture.⁸⁴ Alveolar rupture allows air from the alveolus to enter the pulmonary interstitium where it can dissect along the perivascular sheaths toward the mediastinum. This can lead to pneumothorax, pneumomediastinum, pneumoperitoneum, or subcutaneous emphysema^85,86 (Fig. 47.3). Bronchopleural fistula, tension pneumothorax, tension lung cyst, and subpleural air cyst have also been reported but are less common.⁸⁷

Figure 47.3 Chest computed tomography revealing extensive subcutaneous emphysema (arrows) from the lower neck to the upper abdomen and pneumomediastinum (thick arrows). (From Lai JI, Po-Chou L, Wang WS, et al: Barotrauma related extensive pneumothorax, pneumomediastinum, and subcutaneous emphysema in a patient with acute respiratory distress syndrome with low tidal volume. Postgrad Med J 2010;86:567-568.)

In a multicenter prospective cohort study of 5183 mechanically ventilated patients, the incidence of PBT was 3%.⁸⁸ Asthma, chronic interstitial lung disease, and acute respiratory distress syndrome (ARDS) were identified as independent risk factors for barotrauma. Other studies have also demonstrated that acute lung injury (ALI) and ARDS are independent risk factors for PBT.^89,90 Elevated peak and plateau pressures have been identified as risk factors.^91,92

Neither open lung strategies using high levels of positive end-expiratory pressure (PEEP) nor recruitment maneuvers have been shown to increase the risk of barotrauma.93,94

Clinical Presentation

The clinical presentation of PBT can vary. With pneumothorax, patients may complain of dyspnea or chest pain. Physical findings can include tachycardia, tachypnea, hypertension, or oxyhemoglobin saturation accompanied by unilateral reduction of breath sounds. If a tension pneumothorax develops, there may be hypotension and tracheal deviation. Patients with pneumomediastinum may complain of dyspnea and chest or neck pain. Other findings include tachycardia, tachypnea, and hypertension. A crunching sound may be heard during auscultation. Rarely, hypotension from decreased venous return and cardiac output may occur if tension pneumomediastinum develops.⁹⁵ Pneumoperitoneum may manifest itself as abdominal pain. Other physical findings include abdominal distention, tenderness, and tympany. Rarely, abdominal compartment syndrome may develop if the pneumoperitoneum progresses to a tension pneumoperitoneum.⁹⁶ Subcutaneous emphysema generally presents as painless soft tissue swelling. It typically appears in the upper chest, neck, and face. Compression of the affected areas can reveal crepitus. A rare consequence of severe subcutaneous emphysema is compartment syndrome.⁹⁷

Diagnosis

The diagnosis of pneumothorax is suspected when a patient presents with the symptoms and signs described earlier, then confirmed with a portable chest radiograph. An upright chest radiograph has the highest diagnostic yield for pneumothorax, although diagnosis in the intensive care unit (ICU) may be difficult as most patients are semirecumbent or supine.⁹⁸ In a fully upright chest radiograph, a pneumothorax appears as a radiolucent collection between the visceral and parietal pleurae in the superior portion of the chest. In contrast, when a patient is supine, free air collects in the anterior chest, displacing the costophrenic angle inferiorly, often creating a “deep sulcus” sign. The deep sulcus sign refers to a unilateral increase in the apparent size of the costophrenic angle (Fig. 47.4).

Figure 47.4 Supine chest radiograph of a neonate illustrates the deep sulcus sign with abnormal deepening and lucency of the left lateral costophrenic angle (*). (From Kong A: The deep sulcus sign. Radiology 2003;228(2):415-416.)

Bedside ultrasound is being used more readily in the ICU to rapidly diagnose pneumothorax. Utilizing the M-mode, the absence of “lung sliding” is indicative of the presence of a pneumothorax ⁹⁹ (Video 47.1).

Tension pneumothorax is diagnosed clinically when a patient presents with unilateral absence of breath sounds, a shift of the trachea in the direction away from the absent breath sounds, and hemodynamic compromise in the appropriate setting. Immediate intervention is indicated as there is seldom time for a radiographic evaluation. Rapid clinical improvement following empiric aspiration of a suspected tension pneumothorax is diagnostically definitive. Subsequently, a tube thoracostomy is placed for ongoing management.

Pneumomediastinum frequently coexists with pneumothorax. It is usually diagnosed with a portable chest radiograph. It typically appears as radiolucent streaks in the mediastinum (Fig. 47.5).

Figure 47.5 Chest radiographs revealing the presence of subcutaneous emphysema, pneumomediastinum, and pneumoperitoneum (arrows). (From Alexiou K, Sakellaridis T, Sikalias N, et al: Subcutaneous emphysema, pneumomediastinum and pneumoperitoneum after unsuccessful ERCP: A case report. Cases J 2009;2:120.)

Pneumoperitoneum is diagnosed with a chest radiograph less than one third of the time. A suspected pneumoperitoneum is best evaluated by chest CT.¹⁰⁰ The patient should remain in position for 5 to 10 minutes before the radiograph is taken. This allows time for air to collect in a sufficient volume to be detected radiographically. Pneumoperitoneum may be identified on a supine abdominal radiograph (see Fig. 47.5). Free air accumulates anteriorly when the patient is supine and on a chest or abdominal radiograph may present in several ways. Gas appearing on both sides of the bowel wall is referred to as Rigler’s sign. Gas outlining the peritoneal cavity is known as the football sign. Gas outlining the medial umbilical folds is called an inverted V sign. Gas may also outline the falciform ligament or localize in the right upper quadrant.¹⁰¹

Subcutaneous emphysema is often found by identifying crepitus during physical examination. On chest radiograph of areas of tissue swelling, it can appear as radiolucent streaks throughout the subcutaneous tissue and muscle (see Fig. 47.5).

Prevention

To prevent barotrauma, it is generally recommended that plateau airway pressure be maintained at or below 35 cm H₂O. Plateau pressure is the most indicative of the alveolar pressure and therefore is the measure of greatest concern for the prevention of PBT. Lower plateau airway pressures have been associated with a lower incidence of PBT. A threshold pressure appears to exist at 35 cm H₂O, above which there is a higher incidence of barotrauma. A meta-analysis of 14 clinical trials demonstrated a strong relationship between PBT and a plateau airway pressure greater than 35 cm H₂O or a static compliance less than 30 mL per cm H₂O.¹⁰² There have not been direct comparisons between management targeting a plateau airway pressure or peak airway pressure. Peak airway pressure is likely a less reliable predictor of PBT given the conflicting data.^103–109

Management

The best treatment for PBT is early recognition, and immediate attempts should be made to reduce plateau airway pressure.⁸³ This may require lowering the tidal volume or PEEP, as well as increasing sedation, administering neuromuscular blockade, or advancing treatment of the underlying condition. In cases of pneumothorax while on a mechanical ventilator, there is no high-quality evidence that supports routine insertion of chest tubes for all patients. However, more than 30% of pneumothoraces in mechanically ventilated patients progress to tension pneumothoraces, indicating that these patients must be monitored closely. Treatment for mechanically ventilated patients who develop a pneumomediastinum, pneumoperitoneum, or subcutaneous emphysema is generally supportive unless there is evidence of tension pneumomediastinum or compartment syndrome from pneumoperitoneum or subcutaneous emphysema.⁹⁵

Prognosis

PBT appears to be associated with increased mortality rate, even though barotrauma is not a direct cause of death in most patients. In a multicenter prospective cohort study, patients with barotrauma had a significantly higher mortality rate (51% versus 39%), a longer length of ICU stay (median 9 versus 7 days), and a longer duration of mechanical ventilation (median 6 versus 4 days) than patients without barotrauma.⁸⁸ Mortality rate may be related to the severity of the PBT. In one retrospective cohort study of 1700 mechanically ventilated patients, the mortality rate approached 100% when PBT caused a large (>500 mL per breath) bronchopleural fistula.¹⁰⁹ High-frequency jet ventilation is FDA (Food and Drug Administration) approved for the management of large bronchopleural fistulas, but this may be outweighed in some patients by increased plateau airway pressure (alveolar pressure), decreased oxygenation, or worse hypercapnia.¹¹⁰

Pneumothorax After Fiberoptic Bronchoscopy and Needle Biopsy of the Lung

Multiple literature reviews have documented the relative safety of fiberoptic bronchoscopy (FOB) with transbronchial biopsy. One review of more than 9000 such procedures found that the rate of pneumothorax was 1.9%.¹¹¹ An immediate postbronchoscopic chest radiograph rarely provides clinically useful information, and in FOB without transbronchial biopsy an immediate postbronchoscopy radiograph is not necessary.^112,113 Another study in 2006 concluded that in asymptomatic patients, routine radiograph after transbronchial biopsy is not necessary.¹¹⁴ It was determined that certain patient populations should have routine radiographs performed after FOB with transbronchial biopsy: comatose or mentally retarded patients, patients receiving positive-pressure ventilation, patients with severe respiratory compromise as a result of disease or surgery, patients with bullous disease, patients who complain of chest pain, and outpatients. Pneumothorax after bronchoalveolar lavage without biopsy is extremely rare. The complication of pneumothorax after transbronchial needle aspiration is also low.¹¹⁵

Pneumothorax is the most common complication of needle aspiration or biopsy of the lung. It has been reported to occur in 17% to 26.6% of patients.116–119 The chest tube insertion rate is much lower, ranging from 1% to 14.2%.^116–119 Risk factors for the development of biopsy-related pneumothorax include the presence of COPD, the absence of a history of ipsilateral surgery, small lesion size, a long needle path, and repeated pleural puncture.^116–121 Enlarging or symptomatic pneumothorax can be managed by manual aspiration or placement of a small-caliber chest tube.¹²⁰

Delayed pneumothorax after percutaneous fine-needle aspiration has been reported. A study by Choi and colleagues ¹²² reported on their series of 458 patients who had undergone transthoracic needle biopsy. A follow-up chest radiograph was obtained immediately and at 3, 8, and 24 hours after the biopsy procedure. A pneumothorax that developed after 3 hours was defined as delayed pneumothorax. Pneumothorax developed in 100 of the 458 patients (21.8%), and delayed pneumothorax developed in 15 patients (3.3%). Female gender and absence of emphysematous changes correlated with an increased rate of delayed pneumothorax.

Pneumothorax After Thoracentesis

According to a 1998 National Center for Health Statistics study,¹²³ physicians perform an estimated 173,000 thoracenteses annually in the United States. Iatrogenic pneumothoraces resulting from thoracentesis increase morbidity rate, mortality rate, and length of hospitalization. Previous reports indicated chest tube insertion may be required in up to 50% of cases with a mean duration of placement of approximately 4 days.^124,125 Gordon and colleagues¹²⁶ performed a systematic review and meta-analysis of 24 studies reporting pneumothorax rates after thoracentesis involving 6605 thoracenteses. The overall pneumothorax rate was 6%. In cases in which pneumothorax developed, 34.1% required chest tube placement. Statistically significant risk factors for developing thoracentesis included performing thoracentesis as a therapeutic procedure as opposed to as a diagnostic procedure; the presence of cough, dyspnea, or chest pain during the procedure; and witnessing the aspiration of air during the procedure.¹²⁶ Although not statistically significant, other possible predictors included the need for two or more needle insertions and concurrent mechanical ventilation.¹²⁶ Ultrasonography guidance,^127–129 more experienced operators,¹³⁰ and fewer needle passes conferred lower complication rates,¹³¹ which paralleled findings from central venous catheter insertion studies. Various mechanisms may explain the pneumothoraces that occur after thoracentesis: the lung may be punctured at the time of needle entry or after the fluid has been withdrawn, or a small amount of air may be drawn into the chest during aspiration or along the needle track if high negative intrapleural pressure develops.¹³²

Pneumothorax Resulting from Nasogastric Feeding Tubes

Small-bore Silastic feeding tubes are being used with increasing frequency for short- and long-term enteral hyperalimentation. The first reported case of pneumothorax as a complication of passing a narrow-bore feeding tube was in 1978.¹³³ This once rare complication has now become more common.^134–136 Narrow-bore feeding tubes are particularly likely to give rise to pneumothorax because of the tube’s small diameter (2.7 mm), self-lubricating properties, and wire stylet. These factors allow undetected entry of the tube into the tracheobronchial tree, perforation of pulmonary tissue, and lodging in the pleural cavity.¹³⁷ Other factors that increase the risk of a misplaced feeding tube include the presence of an endotracheal or tracheostomy tube (these may increase pulmonary passage of the tube by preventing glottis closure and perhaps by inhibiting swallowing), altered mental status, denervation of airways, esophageal stricture, enlargement of the heart, and neuromuscular weakness.¹³⁸ The clinical signs commonly used to determine correct placement of the feeding tube may be misleading. Normally, to confirm the correct placement of a feeding tube in the stomach, a small amount of air is injected. This produces a characteristic gurgle in the left upper quadrant of the abdomen, but a “pseudoconfirmatory gurgle” with a feeding tube in the chest has been reported.¹³⁹ Aspiration of large amounts of fluid through the tube is also taken to be a test of correct placement into the stomach, but delayed aspiration of a large quantity of undigested feeding solution from the pleural space, mistaken for gastric contents, has been reported.¹⁴⁰

Pneumothorax After Percutaneous Dilational Tracheostomy

Percutaneous dilational tracheostomy (PDT) was first described in 1985 by Ciaglia and colleagues.¹⁴¹ A case series described subcutaneous emphysema and pneumothorax as complications after percutaneous tracheostomy in a series of 326 cases.¹⁴² Their review of the literature showed that the incidence of subcutaneous emphysema was 1.4% and that of pneumothorax was 0.8%. Findings associated with pneumothorax included difficult PDT and the use of a fenestrated cannula.

Special Situations

Pneumothorax ex Vacuo

Pneumothorax after partial resolution of total bronchial obstruction,¹⁴³ as a complication of lobar collapse,¹⁴⁴ and after therapeutic thoracentesis for malignant effusions¹⁴⁵ has been described. Acute lobar collapse results in a sudden increase in negative pleural pressure surrounding the collapsed lobe. Although the parietal and visceral pleural surfaces remain intact, the gas originating from the ambient tissues and blood is drawn into the pleural space, producing a pneumothorax called pneumothorax ex vacuo. Recognition of this type of pneumothorax is crucial because managing it requires relieving the bronchial obstruction rather than inserting a chest tube. The diagnosis of trapped lung requires documentation of chronicity and absence of pleural inflammation, pleural malignancy, or endobroncial lesion. The pathognomonic radiographic sign of a trapped lung is the pneumothorax ex vacuo, characterized as a small to moderate-sized air collection after evacuation of effusion.¹⁴⁶

The classic signs of a tension pneumothorax are deviation of the trachea away from the side with the tension, an increased percussion note, and a hyperexpanded chest that moves little with respiration. Radiographically, tension pneumothorax shows a distinct shift of the mediastinum to the contralateral side and flattening or inversion of the ipsilateral hemidiaphragm (Fig. 47.6). Clinically unstable patients should undergo immediate needle decompression followed by chest tube insertion. Decompression is performed by advancing a standard 14- or 16-gauge intravenous catheter into the pleural space at the junction of the midclavicular line and the second or third intercostal space. The needle is advanced until air can be aspirated into a syringe connected to the needle. The needle is withdrawn and the cannula is left open to air. An immediate rush of air out of the chest indicates the presence of a tension pneumothorax. The maneuver essentially converts a tension pneumothorax into a simple pneumothorax. A chest tube can then be placed.

Figure 47.6 Chest radiograph of a left tension pneumothorax in a trauma patient. Note the mediastinal shift to the right, widened rib spacing, and posterior rib fractures on the left. A flattening of the left hemidiaphragm is also present (not shown). (From Barton E: Tension pneumothorax. Curr Opin Pulm Med 1999;5(4):269.)

Clinical Features

PSP usually occurs when the patient is at rest.¹⁵⁵ Patients are typically in their early 20s when presenting with PSP, which is rare after age 40. Chest pain and dyspnea are the two main symptoms associated with the development of pneumothorax. One series evaluated 39 patients who presented with one of the two symptoms and 64% of them had both.¹⁵⁶ The pain is generally reported as ipsilateral, which usually resolves spontaneously within 24 hours.⁴⁰ The degree of dyspnea depends on the size of the pneumothorax and the condition of the underlying lung. Cough, malaise, orthopnea, and hemoptysis may also be presenting symptoms.

Physical examination can be normal in small pneumothoraces. Possible physical findings when a large pneumothorax is present include decreased chest excursion on the affected side, diminished breath sounds, and hyperresonant percussion. There may also be subcutaneous emphysema. Labored breathing accompanied by hemodynamic compromise (tachycardia or hypotension) suggests a possible tension pneumothorax, which necessitates emergency decompression. Tension pneumothorax occurs due to the presence of a ball-valve mechanism; air enters the pleural cavity but cannot escape. As a result, positive pressure builds up. As the tension continues to increase, the diaphragm is flattened, the mediastinum is shifted to the opposite side, and ultimately cardiopulmonary collapse results.

Hypoxemia is common because collapsed and poorly ventilated portions of lung continue to receive significant perfusion. However, hypercapnia is unusual because underlying lung function is relatively normal and adequate alveolar ventilation can be maintained by the contralateral lung.¹⁵⁷ Acute respiratory alkalosis may be present if pain, anxiety, or hypoxia is substantial.

In certain situations, the symptoms of pneumothorax may have an atypical presentation and therefore require a high index of suspicion. During a transbronchial biopsy, a patient may complain of pleuritic chest pain followed by dyspnea. A pneumothorax after a subclavian vein catheterization may present with progressive dyspnea and an alteration of vital signs. In a mechanically ventilated patient, the initial presentation may include hypotension, new-onset respiratory distress, unilateral decrease in breath sounds, a decrease in static and dynamic compliance, and worsening oxygenation.41,158,159

Simultaneous bilateral pneumothoraces is a rare condition because, in humans, the left and right pleural spaces are completely separated. Patients can develop a persistent pleuro-pleuro channel after undergoing a median sternotomy, mediastinal surgery, or heart or heart-lung transplant surgery. This condition has been dubbed “iatrogenic buffalo chest” because the North American buffalo is one of few mammals that have communicating pleural spaces.¹⁶⁰ A unilateral thoracic procedure in this situation has been described to cause bilateral pneumothoraces^161,162 and “shifting pneumothorax.”¹⁶³ Simultaneous bilateral spontaneous pneumothorax (SBSP) has been described in a case series with 12 patients.¹⁶⁴ Of the 12 patients, 5 had no underlying lung disease. In 7 patients, SBSP was secondary to pulmonary metastases, histiocytosis, undefined interstitial pulmonary disease, tuberculosis, pneumonia, and COPD.

Electrocardiographic Features

The presence of a pneumothorax may lead to distinct electrocardiographic changes, which can be mistaken for myocardial ischemia or infarction. Most findings have been described for left-sided pneumothorax. Poor R wave progression in the anterior precordial leads with a decrease in R wave from V₄ to V₅, rightward shift of frontal axis, diminution of precordial R voltage, decrease in QRS amplitude, and precordial T-wave inversion have all been described.165–167 The absence of ST-segment elevation and a significant Q wave and reversal of electrocardiographic changes in the sitting position suggest pneumothorax. In right-sided pneumothorax, there is a loss of S wave in lead V₂ and prominent R-wave voltage, which may mimic posterior wall myocardial infarction.¹⁶⁸

Diagnostic Imaging Modalities

Radiographic Signs

Chest radiography and CT are the first-line imaging modalities used to identify a pneumothorax. The main feature of a pneumothorax on a chest radiograph is a white visceral pleural line. This line separates the visceral pleura from the parietal pleura by a collection of gas (Fig. 47.7). A pneumothorax may be identified using an upright, supine, or lateral decubitus chest radiograph. The lateral decubitus view is the most sensitive, and the supine view is the least sensitive.

Figure 47.7 Radiograph of right lung pneumothorax. Arrow points to collapsed lung.

Upright Chest Radiograph

In an upright patient with a pneumothorax, most pleural gas accumulates in an apicolateral location. The visceral pleural line appears either straight or convex toward the chest wall. As little as 50 mL of pleural gas may be seen on a chest radiograph.¹⁶⁹ Although there is generally a loss of lung volume with a pneumothorax, the collapsed lung preserves its translucency because hypoxic vasoconstriction diminishes the blood flow to the collapsed lung. The value of obtaining an expiratory chest radiograph has been overstated. Inspiratory and expiratory upright chest radiographs detected pneumothorax with equal sensitivity.¹⁷⁰

Supine Chest Radiograph

In a supine patient with a pneumothorax, most pleural gas accumulates in a subpulmonary location. A “deep sulcus” sign occurs when gas outlines the anterior pleural reflection, the costophrenic sulcus, and the anterolateral border of the mediastinum (see Fig. 47.4). Rarely, pleural gas can accumulate in the phrenicovertebral sulcus. The visceral pleural line may be seen at the lung base and has a concave contour. Around 500 mL of pleural gas is needed in order to definitively diagnose pneumothorax on a supine chest radiograph.¹⁶⁹

Lateral Decubitus Chest Radiograph

A pneumothorax is most easily detected with a lateral decubitus view. Most pleural gas in this position accumulates in the nondependent lateral location. The visceral pleural line appears as a straight or convex line toward the chest wall. As little as 5 mL of pleural gas may be visible on a lateral decubitus view.¹⁶⁹

Computed Tomography

CT scanning is the most accurate imaging modality for the detection of pneumothorax although it is generally not the initial option. This method can identify small amounts of intrapleural gas, atypical collections of pleural gas, and loculated pneumothoraces. Complex pleural disease such as pleural effusion and cystic lung disease is optimally displayed by CT scanning.¹⁷¹

Pulmonary Ultrasonography

Ultrasound was first used to detect pneumothorax in a horse in 1986 and then in humans shortly thereafter.¹⁷² In a normal lung, the visceral and parietal pleurae are adjacent, and ultrasound shows shimmering or sliding at the pleural interface during respiration.¹⁷³ The absence of “lung sliding” indicates a pneumothorax. Comet tails are an ultrasound artifact that arises when ultrasound encounters a small air-fluid interface (Fig. 47.8). The presence of “sliding lung” and “comet tail” artifacts appear to reliably rule out pneumothorax (Video 47.1). The presence of a “lung point” sign is nearly 100% specific for the detection of pneumothorax. Here the visceral pleura is seen to be intermittently coming into contact with the chest wall during inspiration. The lung point sign may also be helpful in determining the actual size of the pneumothorax (Fig. 47.9). A review of four prospective studies found the sensitivity and specificity of ultrasound for pneumothorax to range from 86% to 98%, which was superior to supine chest radiography (sensitivity 28-75%).¹⁷⁴ A small pneumothorax may be missed with ultrasound, and patients with blebs or scarring may have a false-positive finding.¹⁷⁵

Figure 47.8 Rib shadows (R) are visible as bright reflectors with distal shadow. The pleura (* *) is a bright echogenic line beneath the ribs. Comet tail artifacts (arrows) arise from normal pleura reflecting sound waves. (From Mt. Sinai Emergency Ultrasound Division Tutorials. Accessed at http://sinaiem.us/tutorials/pneumothorax.)

Figure 47.9 Lung point sign. B-mode depicting the lung point: Sliding lung touching the chest wall. (From Husain LF, Hagopian L, Waymen D, et al: Sonographic diagnosis of pneumothorax. J Emerg Trauma Shock 2012;5:76-81.)

Differential Diagnosis: Conditions Mimicking Pneumothorax

Large subpleural bullae can mimic a loculated pneumothorax. Bullae can be distinguished from pneumothorax due to the fact that only bullae typically have a medial border that is concave to the chest wall.¹⁷⁶ Exceptions to this distinction occur with subpulmonary collections of gas, loculated collections of gas, and pleural adhesions. In trauma cases, the stomach can herniate into the chest following rupture of the left hemidiaphragm, and a gas-filled stomach may be mistaken for a loculated pneumothorax. This can be disastrous if drainage with a thoracostomy tube is attempted. A skinfold can generally be distinguished from a pneumothorax by careful evaluation of the radiograph. Skinfolds generally extend beyond the rib cage, stop short of the ribs, and gradually increase in opacity with an abrupt dropoff at the edge of the image. Blood vessels often extend beyond the skinfold.¹⁷⁷

Management

Figure 47.10 represents an algorithmic approach to the management of pneumothorax.

Figure 47.10 Reexpansion pulmonary edema. (From Tung YW, Lin F, Yang MS, et al: Bilateral developing reexpansion pulmonary edema treated with extracorporeal membrane oxygenation. Ann Thorac Surg 2010;89:1268-1271.)

Management of the First Episode of Pneumothorax

Initial management is directed at removing air from the pleural space followed by preventing recurrence. Approaches for the management of the initial episode include observation, supplemental oxygen, simple aspiration of the pneumothorax, and tube thoracostomy. The choice of therapy in a given patient depends on various factors such as size of the pneumothorax, whether the pneumothorax is primary or secondary, the condition of the lungs, the clinical stability of the patient, the outcome of the patient, and whether the pneumothorax has occurred in a special setting. Various guidelines for managing pneumothorax have been published.178,179

Estimating the Size of a Pneumothorax

Determining the size of a pneumothorax is difficult. The average interpleural distance (AID) approximates the size of a pneumothorax from a frontal chest radiograph by taking the sum of the distances in millimeters between the ribs and the visceral pleura at the apical, midthoracic, and basal levels and then dividing the sum by three. Another method is called the Light Index. It uses the following calculation to estimate the size of a pneumothorax:

D_L is diameter of the collapsed lung cubed.

D_H is diameter of hemithorax on collapsed side cubed.

Both methods express the size of the pneumothorax as a percentage, although the Light method better correlates with the amount of pneumothorax gas removed by suction.180,181

These methods are difficult to apply and tend to underestimate the size of a pneumothorax. As a result, some clinicians tend to describe a pneumothorax as large or small rather than utilize percentages. The American College of Chest Physician guidelines defines a small pneumothorax as less than 3 cm in apex-to-cupola distance.¹⁷⁸ British Thoracic Society guidelines define a pneumothorax as small if the distance from chest wall to visceral pleural line is less than 2 cm. They define a large pneumothorax if the distance from the chest wall to the visceral pleural line is 2 cm or greater.¹⁷⁹

Treatment Options

Supplemental Oxygen

The choice of treatment depends on patient characteristics and clinical circumstances. Patients who are clinically stable and are having their first PSP can be observed with administration of supplemental oxygen if their pneumothorax is small (≤2 to 3 cm between the lung and chest wall on a chest radiograph).¹⁸² Supplemental oxygen is used to facilitate reabsorption of pleural air, and its importance should not be underestimated. The absorption of gas depends in part on the gradient between the partial pressure in the capillaries and that in the pleural space. On room air, the net gradient is only 54 mm Hg, whereas it exceeds 550 mm Hg when the patient is on 100% oxygen.¹⁸⁰ A normal rate of reabsorption is 1.25% of the volume of the hemithorax per 24 hours.⁷ The rate of reabsorption increases sixfold if humidified 100% oxygen is administered.¹⁸³ Therefore, hospitalized patients with any type of pneumothorax who are not subjected to aspiration of air or tube thoracostomy should be treated with supplemental oxygen at high concentrations.¹⁸⁴

Removal of Air from Pleural Space

In a patient whose pneumothorax is large (more than 20-25%), progressive, tension type, or symptomatic or who has an underlying chronic lung disease, is on a ventilator, or has a recurrent pneumothorax, the pleural space air should be removed. Several therapies have been developed for this purpose.

Aspiration

Simple aspiration is most easily accomplished by using a commercially available thoracentesis kit. An 18-guage needle with an 8 to 9F catheter is inserted in the second intercostal space in the midclavicular line. Once the catheter is inserted into the pleural space, the catheter is threaded deeper into the pleural space, and then the needle is withdrawn. Air is manually withdrawn through the indwelling catheter until no more can be aspirated. If the lung has not expanded after 4 L have been aspirated, then it is assumed there is a persistent air leak. Thoracoscopy should then be performed. A chest tube should be inserted if thoracoscopy is not readily available.

Once no further air can be aspirated, one of two methods may be approached.¹⁸⁵ A closed stopcock can be attached and the indwelling catheter secured to the chest wall. After 4 hours, a chest radiograph should be obtained and if there is adequate lung expansion, the catheter can be removed. Following another 2 hours of observation, another chest radiograph should be performed. If the lung remains expanded on this chest radiograph, the patient can be discharged.¹⁸⁶ Alternatively, the catheter can be left in place and attached to a Heimlich (i.e., one-way) valve. The patient can then be discharged with follow-up within 2 days.^178,187 One advantage of aspiration over tube thoracostomy is that the patient need not be hospitalized whether the catheter is removed after aspiration or left attached to the Heimlich valve. There is a lower morbidity rate compared to tube thoracostomy and the procedure is better tolerated. Outcomes have been found to be similar between thoracostomy and aspiration. In a meta-analysis of three randomized, controlled trials (194 patients) that compared aspiration versus tube thoracostomy, aspiration resulted in shorter hospitalization stays and similar clinical outcomes.¹⁸⁸ In another randomized trial, 137 patients who had a first episode of PSP were assigned to receive manual aspiration versus tube thoracostomy. The groups had similar rates of immediate (62 versus 68%) and 1-week success (89 versus 88%). Aspiration was associated with a shorter hospital stay (1.8 versus 4 days).¹⁸⁹

Tube Thoracostomy

If necessary, most patients with PSP can be managed with a small chest tube (≤22F) or chest catheter (≤14F).190,191 In the absence of trauma and with good aseptic technique, prophylactic antibiotics are not recommended.¹⁹² The preferred location for insertion of the chest tube is via an incision at the fourth or fifth intercostal space in the anterior or midaxillary line.^193–195 In men, this corresponds to the nipple line and in women, to the inframammary crease. It is important to direct the tube anteriorly because the tube tends to track between the lobes in patients who have complete fissures. If this happens, the tube may get walled off by the lung and cease functioning. The second intercostal space in the midclavicular line has been suggested as an alternative site for tubes, but this requires placement through the pectoralis muscle. This chest tube site is more painful for the patient and the tube is more difficult to dress and manage. Once an insertion site is identified, the tube is inserted using blunt dissection and secured in place.

The chest tube can then be connected to a water seal device, with or without suction and left in position until the pneumothorax resolves. Once the air leak has resolved, the lung has fully expanded, and the pleural air removed, then the chest tube can be removed in a sequential fashion. The chest tube can generally be removed if there is no visible air leak present and air does not accumulate when suction is removed. If there is any question as to whether an air leak has resolved, a “clamp trial” can be performed. This involves clamping the chest tube and performing a chest radiograph repeated at intervals (e.g., 2, 6, and then 12 hours). If air does not reaccumulate, the tube can be removed.

Percutaneous Pneumothorax Catheters and Thoracic Vents

Alternatives to tube thoracotomy involve using small-lumen catheters or thoracic vents (one-way valve feature). Small catheter tubes have the advantages of ease of insertion, good response, and low incidence of complications. Liu and colleagues reported that in their study using pigtail catheters in 50 patients versus traditional chest tubes in 52 patients that the pigtail drainage was no less effective than the traditional chest tube.¹⁹⁶ Complications can include catheter failure from kinking, malposition, inadvertent removal by the patient, and occlusion of the tube or valve by pleural fluid. A thoracic vent can also be used to manage a simple pneumothorax.^197,198 It is inserted in the second intercostal space in the midclavicular line. This device has the advantages of a urethane tube that does not kink, a self-contained one-way valve, and a unique signal diaphragm that reflects pleural pressure. This device is not suitable for use in patients who are expected to have large-volume or protracted air leaks.

Thoracoscopy

VATS is an effective treatment of PSP.199–201 Pleurodesis is created by pleural abrasion or a partial parietal pleurectomy. When necessary, an endoscopic stapler can be used to resect bullae.^202–205

Persistent Air Leak and Bronchopleural Fistula

If a lung is at least 90% inflated but an air leak is present after 3 days, more aggressive treatment may be warranted. The simplest approach is to attach the chest tube to a unidirectional flutter valve such as a Heimlich valve. This allows rapid discharge of the patient with subsequent outpatient follow-up. An alternative approach is to perform an autologous blood patch.206,207 This involves withdrawing blood from the patient’s peripheral vein and aseptically infusing the blood into the pleural space through the chest tube. The ideal amount of blood to infuse is not known. The range in different series has been 24 to 200 mL. After infusion of the blood, the tubing from the chest tube is draped over a hook approximately 60 cm above the patient’s head and then down to a water seal device on the floor. The chest tube is then removed 24 hours after cessation of the air leak. The most serious side effect is empyema, which occurred in 9% of patients in one series.²⁰⁸ Lastly, if the lung is less than 90% expanded and the patient has a persistent air leak, the preferred intervention is VATS. An air leak persisting for more than 7 days is termed a bronchopleural fistula and can occur in up to a third of pneumothorax cases.²⁰⁹ After 7 days of a persistent air leak, tube thoracostomy is deemed to have failed and more definitive treatment such as surgery or pleurodesis can be planned.

Recurrence Prevention

Once the initial episode of pneumothorax has resolved, the decision to prevent future pneumothoraces must be made. Different recurrence rates have been reported in the literature; from 20% to 52% after the first PSP.210–212 In the following groups of patients, further management against recurrence is recommended: recurrent pneumothorax, patients with chronic air leak, patients with large bullae, patients who live in remote areas, and patients in which a recurrence could be a hazard (e.g., airline personnel or divers). The following are established risk factors for recurrence: more than one previous episode, COPD, air leak for more than 48 hours after first episode, and large cysts seen on radiograph. The following are possible risk factors for recurrence: nonoperative management of first episode (versus tube drainage) and tube drainage for only 24 hours during first episode (versus 3 to 4 days). Further management in these high-risk groups is aimed at preventing recurrence. Therapies to prevent recurrence include chemical pleurodesis, VATS, or surgical thoracotomy.

Chemical Pleurodesis

In patients who are unable or unwilling to undergo VATS, pleurodesis (adhesion of visceral and parietal pleura) can be done by introducing the sclerotic agent via the chest tube. Tetracycline had been used for pleurodesis,²¹³ but sterile tetracycline is no longer available. As a result, intrapleural instillation of doxycycline has been used as an alternative for pleurodesis.²¹⁴ Intrapleural doxycycline can be painful, so it is recommended that patients be premedicated with analgesics or anxiolytics. Talc slurry, which is composed of finely powdered magnesium silicate, can also be used for pleurodesis.^215–217 Recurrence rates after treatment vary between 5% and 8%. Controversy exists whether talc should be used as a sclerosant in young, otherwise healthy individuals due to safety concerns and fear of long-term complications. Intrapleural injection of talc for malignant pleural effusions has been associated with development of ARDS in 1% to 2% of patients.²¹⁸ Extensive pleural thickening and calcifications were reported in another patient years after treatment.²¹⁹ However, several studies support the safety of talc pleurodesis for prevention of recurrent pneumothorax.^215,220,221

Video-Assisted Thoracoscopic Surgery Pleurodesis

VATS is effective not only in the treatment of spontaneous pneumothorax but also in the prevention of recurrent pneumothorax.222,223 The rate of recurrence is less than 5% after VATS with bleb/bullae resection and pleurodesis. Mechanical pleurodesis with dry gauze, chemical pleurodesis with talc, and laser ablation of the parietal pleura are among the techniques used.

Surgical Thoracotomy

Surgical management for the first episode of spontaneous pneumothorax is indicated under the following circumstances: 3% to 4% of patients have a persistent leak resulting from a large fistula that needs to be closed surgically; about 5% of patients have frank hemothorax and surgical intervention is required to control the bleeding; and a trapped lung that fails to reexpand may require decortication.

The indications for open thoracotomy are the same as those for VATS. Thoracoscopy has virtually replaced open thoracotomy in the management of spontaneous pneumothorax due to shorter hospitalizations and less postoperative pain.224,225 Thoracotomy is recommended only if thoracoscopy is unavailable or has failed.

Management Under Special Circumstances

Secondary Spontaneous Pneumothorax

Patients with SSP should be hospitalized owing to their diminished pulmonary reserve from their underlying lung disease. Patients with a small pneumothorax (≤2 cm between the lung and chest wall on a chest radiograph) who are clinically stable may be observed. Patients with a large pneumothorax or who are clinically unstable should have a chest tube placed. Tube thoracotomy is generally preferred over needle aspiration because it is more likely to be successful. In one trial, tube thoracostomy was more likely to have the pleural air completely evacuated than with needle aspiration (93% versus 67%).²²⁶ About 80% of patients with SSP will have lung expansion and cessation of their air leak within 7 days after tube thoracostomy.^227,228 Patients who are on mechanical ventilation or who are at risk for a large air leak should be managed with a 24 to 28F chest tube. A smaller chest tube (16 to 22F) is preferred for most other patients. The chest tube should be connected to a water seal device with or without suction. In general, the chest tube should remain in place until a procedure is performed to prevent a recurrent pneumothorax. Patients who decline preventive interventions can have their chest tube clamped 12 hours after the last evidence of an air leak. A chest radiograph should be done 24 hours after the last evidence of an air leak, and if the pneumothorax has not recurred, the chest tube can be removed.

Pneumothorax in HIV-Infected Patients

Because the majority of pneumothoraces in HIV-infected patients occurs in association with P. jiroveci, all HIV-infected patients who present with a pneumothorax should undergo a diagnostic evaluation for P. jiroveci infection. P. jiroveci pneumonia–related pneumothorax is complicated by a virulent form of necrotizing subpleural lesions, which result in diffuse air leaks that are refractory to standard treatment.²²⁹ Asymptomatic patients with a small pneumothorax (less than 15-20%) may be observed. Symptomatic patients and those with a larger pneumothorax will need chest tube thoracostomy and those with a persistent air leak will likely need additional therapy with video-assisted thoracoscopy for stapling and pleurodesis. Patients who are poor operative candidates may benefit from bedside pleurodesis.

Pneumothorax in Cystic Fibrosis

Pleurodesis as an initial step in the management of pneumothorax in CF is considered contraindicated because it results in extensive pleural adhesions that jeopardize subsequent lung transplantation.²³⁰ If initial tube thoracostomy does not bring resolution of air leak within 5 days, blebectomy should be performed. If blebectomy is unsuccessful, a definitive pleural ablative procedure should be considered.

Catamenial Pneumothorax and Pneumothorax Complicating Pregnancy

The initial episode is managed in the usual manner. Recurrences, which occur 72 hours before or after menstrual flow, are managed by pleurodesis or hormonal treatment.²³¹ Therapeutic options include oral contraceptive pills, danazol, progestational agents, and gonadotropin-releasing hormone (GnRH) analogs.⁶⁹ Thoracotomy should be considered if the patient is unable to take ovulation-suppressing drugs, has a recurrent pneumothorax while on drugs, or wants to become pregnant. Pneumothorax complicating pregnancy is managed in the usual way, but due to the fact that there is a high rate of recurrence during parturition, thoracotomy with resection of blebs if present should be considered.²³²

Pneumothorax in Air Travelers

The volume of gas is inversely proportional to the pressure at which it is exposed. As barometric pressure falls in the aircraft cabin during ascent, trapped air in any noncommunicating body cavity, such as in a lung bleb or bulla, will expand. Regulatory government agencies, such as the Federal Aviation Administration, have requirements specifying that commercial aircraft cabins be pressurized to simulate an altitude (so-called cabin altitude) of approximately 8000 ft (2438 m). It is estimated that the volume of air in a noncommunicating body cavity will increase by approximately 38% upon ascent from sea level to the maximum “cabin altitude” of 8000 feet (2438 m).²³³ For patients who develop signs and symptoms of a pneumothorax in-flight, administration of supplemental oxygen is the most important intervention. For patients in respiratory distress, emergency landing at the nearest airport will allow prompt evaluation and insertion of a chest tube, if needed. The optimal length of time to wait after resolution of a pneumothorax is unknown.²³⁴ For patients with a prior pneumothorax, the decision regarding air travel must be made on an individual basis. One must take into consideration the likelihood of recurrence and how well the patient would tolerate a subsequent pneumothorax. A patient with relatively normal lung parenchyma could be permitted to fly 2 weeks after resolution of an iatrogenic pneumothorax. In a patient with severe bullous emphysema, limited cardiopulmonary reserve, and a prior spontaneous pneumothorax, air travel may be contraindicated.

Pneumothorax in Lymphangioleiomyomatosis

Lymphangioleiomyomatosis (LAM) is a rare and often fatal disease that affects predominantly women of childbearing age. The normal architecture of the lung is distorted by multiple small cysts, ranging from 0.1 cm to several centimeters in diameter, with progressive decline in lung function. Spontaneous pneumothorax occurs in 50% of cases. It is often recurrent, can be bilateral, and may necessitate pleurodesis.235,236 Because of the morbidity and cost associated with multiple recurrences, recommendations include definitive intervention at the time of the initial pneumothorax. Pleurodesis in these cases does not preclude successful transplantation.²³⁷

Complications Related to Management

Reexpansion pulmonary edema may occur after rapid reexpansion of a collapsed lung in patients with a pneumothorax. It is typically unilateral ²³⁸ (Fig. 47.11). The pathophysiologic mechanism is unknown. The incidence of reexpansion pulmonary edema initially appeared to be related to the rapidity of lung reexpansion and to the severity and duration of lung collapse. However, a study examining development of reexpansion pulmonary edema following thoracentesis found that it was independent of the volume of fluid removed and pleural pressures, and recommended that even large pleural effusions be drained completely as long as chest pain or end-expiratory pleural pressure less than −20 cm H₂O does not develop.²³⁹ Patients typically present soon after the inciting event, although presentation can be delayed for up to 24 hours in some cases. The clinical course varies from isolated radiographic changes to complete cardiopulmonary collapse. Mortality rates as high as 20% have been described.²⁴⁰ Treatment is generally supportive. Supplemental oxygen is administered and, if necessary, mechanical ventilation is used. The disease is usually self-limited.

Key Points