Pneumothorax and Barotrauma

HISTORY

Pneumothorax (PTX), the accumulation of air in the pleural space, results from a break in the visceral or parietal pleura. Hippocrates was perhaps the first physician to suspect the presence of air in the pleural space in one of his patients, but it was in 1803 that the term pneumothorax was used for the first time.¹ Although Laennec² gave the first clinical description of pneumothorax in 1819, it was not until 1901 that this entity was demonstrated on a chest radiograph published in the Lancet.³ In the eighteenth and nineteenth centuries, pneumothoraces were believed to be the result of tuberculosis. This belief was laid to rest when Kjaergaard,⁴ in 1932, described the occurrence of this condition in otherwise healthy young adults. Definitive therapy for the condition became available with the advent of tube thoracostomy, employed by Hewett in 1876.⁵

INCIDENCE

Weissberg and Refaely⁶ reported on 1199 patients with pneumothorax. Of 865 male and 334 female patients, 60.3% of the pneumothoraces were spontaneous, 33.6% were traumatic, and 6.1% were iatrogenic. Chen and colleagues,⁷ in their university-based teaching hospital ICU, found that of 60 patients who developed pneumothorax while in the ICU, 58% were related to procedures, most commonly thoracentesis.

The reported recurrence rates of pneumothorax vary widely, depending on the type of pneumothorax and the duration of follow-up. A compilation of 11 studies showed that the recurrence rate in “primary” spontaneous pneumothorax (PSP) ranged from 16% to 52% with a mean recurrence rate of 30% in those without definitive preventive treatment.⁸ Table 48-1 categorizes episodes of pneumothorax seen at Nassau University Medical Center, a 530-bed hospital and trauma center in the suburbs of New York City.

Table 48-1.

Episodes of Pneumothorax (PTX) Seen at Nassau University Medical Center

Type of PTX	2001	2002	2003	2004	2005	2006
Spontaneous PTX	20	14	21	15	30	23
Iatrogenic PTX	21	24	27	8	26	20
Traumatic PTX without open wound	44	42	65	68	61	76
Traumatic PTX with open wound	11	10	7	5	6	8
Total	96	90	120	96	123	127

PATHOPHYSIOLOGY

Etiology

Conventionally, PSP has been defined as a pneumothorax that occurs spontaneously in a patient who has no underlying lung disease. However, a condition is unlikely to remain “primary” or “idiopathic” as we gain understanding about this disease process. Diagnoses labeled as “primary” then shift into the category of “secondary.”

Emphysema-Like Changes

Understanding the development of PTX in a patient who has known blebs and bullae is easy. However, computed tomography (CT) can detect abnormalities predisposing to PSP in patients with normal chest radiograph. CT has demonstrated emphysema-like changes (ELCs) in patients with PSP. Bense and others⁹ reported on 27 nonsmoking cases of spontaneous pneumothorax (SP) who were not deficient in alpha-1 antitrypsin. In 22 cases (81%), CT showed ELCs. These changes were found mainly in the upper and peripheral regions. No ELCs were detected in the control group. Other investigators10, 11 have also reported similar findings on CT in their cases of PSP.

Pleural Porosity

Although the previously mentioned studies support the role of ELCs in the pathogenesis of PSP, ELCs are not the sole cause of PSP.12, 13 Air leak is not seen at the site of ruptured ELC in each patient during surgical intervention for PSP. Moreover, an air leak can be present in areas where no ELCs are seen. This has led to the concept of “pleural porosity.”14, 15 Noppen and colleagues¹⁴ have described a patient with recurrent PSP in whom inhalation of aerosolized fluorescein followed by autofluorescence thoracoscopy allowed in vivo localization of various areas of extensive subpleural fluorescein accumulation, which were not visible with normal white thoracoscopy. This has led to the concept of “porous” pleura.¹⁵

Smoking

In a study on 138 Swedish patients, Bense and colleagues¹⁶ found that smoking increased the risk of developing PSP 9-fold in women and 22-fold in men. Although cessation of smoking appears to reduce the risk of recurrence,¹⁷ continued smoking increases the risk of recurrence.¹⁸ Cottin and colleagues¹⁹ found that in 79 smokers who underwent surgery for recurrence or persistence of PSP, 70 (88.6%) had evidence of respiratory bronchiolitis. Smit and colleagues²⁰ performed spirometrically controlled high-resolution CT density measurements in 41 patients with SP and found that the mean lung density was lower in patients with pneumothorax. They hypothesized that peripheral airway inflammation leads to airway obstruction with a check valve phenomenon, causing air trapping and development of pneumothorax. No correlation was found between air trapping and smoking habit or ELCs.

Genetics

Although rare, familial inheritance of pneumothorax has been reported.21, 22 The analyses suggest two possible models of inheritance: an autosomal dominant gene with incomplete penetrance and an X-linked recessive gene. The occurrence of recurrent SP in a Finnish brother and his sisters also raises the possibility of autosomal recessive inheritance.²³ As in SP, patients with Marfan syndrome are tall, and pneumothorax is a common pulmonary complication. Marfan syndrome is caused by the mutation in the 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. Cardy and colleagues²⁴ hypothesized that familial SP is caused by a connective tissue disorder that exhibits mendelian inheritance and postulated FBN1 as the causative gene. Another interesting syndrome in which patients develop SP has been described. Brit-Hogg-Dube (BHD) is an autosomal dominant cancer syndrome characterized by benign skin and renal tumors, pleuropulmonary blebs and cysts, and SP. The gene has been mapped to chromosome 17p11.2 and recently identified, expressing a novel protein called folliculin.25, 26

Effect of Pneumothorax on Cardiopulmonary Physiology

As a result of a breach in the visceral or parietal pleura, air enters the pleural space. When the amount of air is large and the increase in intrapleural pressure great, the mediastinum shifts to the opposite side and the diaphragm is depressed (Fig. 48-1 ). A decrease in vital capacity, functional residual capacity, total lung capacity, and oxygen transfer occurs.²⁷ In a large pneumothorax, the arterial oxygen pressure (Pao ₂) falls and the alveolar-arterial oxygen pressure difference [P(A-a)O₂] increases. The factors that lead to hypoxemia during a large pneumothorax are anatomic shunt,²⁸ hypoventilation,²⁹ and relative overperfusion of partially collapsed, underventilated lungs.³⁰ Anthonisen³¹ reported that in patients with pneumothorax, airway closure occurs at low lung volumes and suggested that this was the main cause of ventilation maldistribution in such patients.

Figure 48-1.

Radiograph of a patient with tension pneumothorax showing shift of the mediastinum to the opposite side.

Animal studies suggest that the progressive hypoxemia with increasing pneumothorax is primarily the result of increasing degrees of pulmonary vascular shunting associated with increasing parenchymal collapse.³²

CLASSIFICATION

The classification given in Box 48-1 combines the circumstances of occurrence of pneumothorax, the etiologic factors, and the state of the underlying lung. When pneumothorax occurs without trauma and is not iatrogenically induced, it is called SP. SP occurring in an otherwise healthy person is called PSP, as mentioned earlier. Secondary SP (SSP) occurs in patients with a variety of underlying lung diseases. Other interesting categories of SP are catamenial pneumothorax, pneumothorax in drug addicts and acquired immunodeficiency syndrome (AIDS) patients, and familial SP.

Box 48-1. Classification of Pneumothorax and Barotrauma.

• A.
  Spontaneous pneumothorax

  • a.
    Primary spontaneous pneumothorax (PSP)

    • 1.
      In healthy young adults
    • 2.
      Familial spontaneous pneumothorax
  • b.
    Secondary spontaneous pneumothorax (SSP)

    • 1.
      Secondary to underlying lung disease
    • 2.
      In drug abusers
    • 3.
      In AIDS patients
    • 4.
      Catamenial pneumothorax
• B.
  Nonspontaneous pneumothorax

  • a.
    Traumatic pneumothorax
  • b.
    Iatrogenic pneumothorax

    • 1.
      Barotrauma and pneumothorax associated with mechanical ventilation
    • 2.
      Accidental

      • During diagnostic procedures: Transbronchial lung biopsy and aspiration, subclavian vein catheterization, thoracentesis, electrophysiologic testing
      • During therapeutic procedures: CPR, surgical tracheostomy, percutaneous tracheostomy, pulmonary function testing, acupuncture, incorrect position of nasogastric tube, secondary to radiation and chemotherapy, laparoscopic cholecystectomy, hyperbaric oxygen
• C.
  Special situations

  • a.
    Pneumothorax ex vacuo
  • b.
    Sports-related pneumothorax
  • c.
    Barotrauma unrelated to mechanical ventilation
  • d.
    Postoperative air spaces
  • e.
    Barotrauma in airplane passengers, pilots, divers, and other causes of barotrauma
  • f.
    Spontaneous pneumothorax following contralateral pneumonectomy
  • g.
    Spontaneous pneumothorax in pregnancy
  • h.
    SARS, CPR

AIDS, acquired immunodeficiency syndrome; CPR, cardiopulmonary resuscitation; SARS, severe acute respiratory syndrome.

Spontaneous Pneumothorax

Primary Spontaneous Pneumothorax

Investigators have found subpleural blebs or bullae at apices on chest radiographs and at thoracotomy in patients with SP.³³ The pathogenesis of these blebs and the factors that lead to their rupture remain controversial.

PSP is classically seen in previously healthy young men with an asthenic body habitus. Melton and colleagues³⁴ found that the incidence of PSP rose with increasing height among adults of both sexes, more so in males. It reached a figure of more than 200 per 100,000 person-years for those 76 inches or taller. It has been suggested that the greater prevalence of SP in tall, thin males is the result of a combination of circumstances. In an extremely long and narrow chest, the apical alveoli are underperfused; such alveoli are more readily torn by gravitational stress. Inherited weakness of connective tissue might also contribute to the pathogenesis, as suggested by the numerous reports of SP in families and concurrent occurrence of SP in twins.³⁵ Morrison and colleagues³⁶ have reported a family exhibiting spontaneous pneumothorax in a father and three offspring and suggested that isolated autosomal dominant pneumothorax may be a distinct entity.

Most patients with SP are heavy smokers. In one series,³⁷ 72% of all patients were smokers. An increase in cigarette consumption during a particular year was followed within 1 to 2 years by an increased incidence of SP; the reverse occurred with decreased cigarette consumption.³⁸ Smoking increases the relative risk of developing SP about 9-fold in women and 22-fold among men, and there is a statistically significant dose-response relationship between smoking and SP.³⁹

Secondary Spontaneous Pneumothorax

Pneumothorax Secondary to Underlying Lung Disease

In adults, SP has been reported to occur as a result of a large variety of diseases including asthma, staphylococcal septicemia, pulmonary infarction, sarcoidosis, idiopathic pulmonary hemorrhage, pulmonary alveolar proteinosis, familial fibrocystic pulmonary dysplasia, tuberous sclerosis, cryptogenic fibrosing alveolitis, eosinophilic granuloma, coccidioidomycosis, echinococcal disease, chronic obstructive pulmonary disease (COPD), Shaver's disease (bauxite pneumoconiosis), lymphangioleiomyomatosis, von Recklinghausen's disease, gastropleural and colopleural fistulas through the diaphragm into the left pleural cavity, radiation therapy to the thorax, Wegener's granulomatosis, cystic fibrosis, acute bacterial pneumonia, and as a complication of the chemotherapy used in the treatment of malignancy and pulmonary metastases from a variety of malignancies.⁴⁰

The most common cause of secondary SP, however, is COPD. SP in COPD patients is a serious complication with excessive morbidity and mortality.8, 41 The clinical presentation of pneumothorax in COPD patients 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 slow to heal, so it is weeks before the tubes can be taken out.⁴²

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 subclavicular or supraclavicular injection (“pocket shoot”) of drugs in the street setting has led to unilateral or bilateral pneumothoraces.43, 44, 45, 46, 47 Douglas and Levison⁴⁷ found that the incidence of pneumothoraces is equal in both sexes and that it is less of a problem in teenagers (because they are unwilling to invade the clearly dangerous territory of neck veins or because they have not yet exhausted the peripheral veins) and in addicts older than 40 years of age (probably because either conservation alters their behavior or they do not survive to their fifth decade). 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. Quite often the pneumothorax is bilateral.43, 45

Pneumothorax in Acquired Immune Deficiency Syndrome Patients

Since the first report of spontaneous pneumothorax in patients with AIDS in 1984 by Wollschlager and colleagues,⁴⁸ numerous other authors49, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60 have reported on the occurrence of pneumothorax in these patients.

SP is an uncommon event (0.06%) in the general population and occurs rarely in association with infectious pneumonia.⁶¹ Spontaneous pneumothorax in patients with AIDS has become the leading cause of nontraumatic pneumothorax in this population.⁶² With the diagnosis of AIDS, a patient's risk of sustaining a nontraumatic pneumothorax increases to 450 times that of general population.⁶³ A high incidence (2% to 9%) has been reported in patients with AIDS and Pneumocystis carinii pneumonia (PCP).58, 59, 64 Pneumocystiscarinii, which was thought to be a protozoan, has been renamed as Pneumocystis jerovici and is now classified as an Archiascomycetous fungus.⁶⁵ Mechanical ventilation and bronchoscopy are quite often required in AIDS patients, and these two factors further increase the chance of pneumothorax occurring in these patients.53, 66 In patients with AIDS, the pneumothorax is frequently bilateral, recurrent, and not responsive to conservative therapy.67, 68 Most often it is related to the infection with P. jerovici, but other infections like Mycobacterium tuberculosis, M. avium intracellulare, pulmonary cytomegalovirus, Pneumococcus organisms,⁵³ or pulmonary toxoplasmosis⁶⁹ may be associated. In a study of 144 patients of AIDS with PCP, the overall mortality was reported to be 21.5%; pneumothorax was found to be one of the seven factors that predicted 90-day mortality.⁷⁰

The exact pathogenesis of the pneumothorax in these patients is not clear. In AIDS patients who have or have had active PCP, large confluent areas of thin-walled blebs, distributed randomly on the surface of each lobe, have been reported.⁵³ It has been postulated that the cystic changes may result from a check-valve mechanism caused by airway inflammation and resultant partial airway obstruction or may be the result of disordered parenchymal architecture secondary to chronic infection and inflammation.54, 55

Various investigators51, 55, 58 have pointed out that the incidence of spontaneous pneumothorax is especially high in those patients who receive aerosolized pentamidine for PCP prophylaxis. This has been attributed to poor distribution of the aerosolized pentamidine at the periphery of the lung, which allows the development of a peripheral necrotizing pneumonitis, producing a bronchopleural fistula with resultant pneumothorax.⁵⁸ Alternately, an ongoing acute infection in inadequately treated areas may eventually result in cystic dilation of distal airway.⁵⁵ Martinez and colleagues⁵¹ have suggested that the sulfite in the isethionate component of the aerosol may cause an irritant cough, resulting in a rupture of the cysts. It has been found that low diffusing capacity of lung for carbon monoxide before pentamidine therapy for secondary prophylaxis is associated with an increased risk of bilateral pneumothoraces and increased mortality in these patients.⁶⁰

Catamenial Pneumothorax

A “catamenial pneumothorax” is defined as a spontaneous or recurrent pneumothorax occurring within 72 hours from the onset of menstruation. Alifano and colleagues⁷¹ described 32 women with spontaneous pneumothorax who had been referred for surgical treatment. In eight cases (25%), the catamenial character of the pneumothorax was recognized by clinical history. In all eight cases, the pneumothorax was recurrent (one to four previous episodes) and right sided. A diaphragmatic abnormality was found in all eight cases. 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 in the chest is through the venous implants that lodge in the lung itself.⁷² Clinical manifestations of thoracic endometriosis include chest pain, dyspnea, and hemoptysis. Bilateral pneumothoraces and concurrent hemothorax, hemoptysis, chest pain, and pneumothorax have been described.⁷³

Nonspontaneous Pneumothorax

Traumatic Pneumothorax

Traumatic pneumothorax most often occurs as a result of penetrating injury but may also occur with closed chest trauma consequent to alveolar rupture from thoracic compression, fracture of a bronchus, esophageal rupture, or rib fractures that lacerate the pleura.74, 75 Traumatic pneu mothorax can be subclassified into open, closed, tension, or hemopneumothorax. A tension pneumothorax needs to be managed immediately by letting the air out with a large-bore needle. Open pneumothorax should have a moist sterile gauze pack placed over the open wound, followed by a chest tube. Hemopneumothorax requires insertion of a chest tube.⁷⁶

Increasing use of computed tomography (CT) scan to evaluate blunt abdominal trauma has revealed a new diagnostic entity that has been called occult pneumothorax. 77, 78, 79, 80, 81, 82 In the series of trauma patients reported by Hill and colleagues,⁸³ there were 67 patients (71 pneumothoraces) who were seen to have a pneumothorax on CT that was not seen on admission chest radiograph. The management of these pneumothoraces is controversial. Wolfman and colleagues,⁸⁴ reporting on 44 occult pneumothoraces, suggested that most small (minuscule) occult pneumothoraces can be managed by close observation. Moderate-sized pneumothoraces can also be managed by observation if the patient is not on a ventilator, but most of the anterolateral pneumothoraces need chest tube placement.

Iatrogenic Pneumothorax

The leading causes of iatrogenic pneumothorax are transthoracic needle aspiration (24% to 36%), subclavian venipuncture (22% to 23%), and thoracentesis (20% to 31%). Positive pressure ventilation has been reported to be the causative factor in only 7% of all iatrogenic pneumothoraces. Most patients require treatment for 4 to 7 days, and hospitalization is prolonged in only a small number of patients because of this complication.85, 86

Barotrauma and Pneumothorax in Mechanically Ventilated Patients

An important complication of mechanical ventilation is barotrauma. In one of the series,⁸⁷ 15 of 430 patients receiving ventilatory support for longer than 12 hours developed pneumothorax. More recently, Lassence and colleagues⁸⁸ reported that iatrogenic pneumothorax occurred in 3% of intensive care unit patients. Risk factors were AIDS, acute respiratory distress syndrome (ARDS), or cardiogenic pulmonary edema at admission, body weight less than 80 kg, central vein or pulmonary artery catheter insertion, and use of inotropic agents during the first 24 hours.

When the lungs are exposed to high volumes, tissue disruption may occur. Air passes along bronchovascular bundles to the lung hilum and then to other interstitial spaces and may enter pleural or pericardial cavities.⁸⁹

In a ventilated patient, a rise in peak and plateau pressures should alert the clinician to the possible complication of pneumothorax.⁹⁰ Petersen and Baier⁹¹ reported a 43% incidence of barotrauma in patients who required a peak airway pressure above 70 cm H₂O. An early radiologic feature and a harbinger of life-threatening barotrauma is the presence of pulmonary interstitial emphysema. Pulmonary interstitial emphysema manifests radiologically as small parenchymal cysts, circular cuffs around larger pulmonary vessels projected end-on (perivascular halos), small dots representing small peripheral vessels surrounded by areas of radiolucency, linear streaks of air radiating toward the hilum, and large cystic collections of air and subpleural air.92, 93 The air, having entered the interstitium, then dissects proximally along bronchovascular sheaths toward the lung hilum and mediastinum. Once in the mediastinum, the accumulated air takes the path of least resistance and may produce subcutaneous emphysema, pneumopericardium, pneumoperitoneum, or retroperitoneum (Fig. 48-2 ). If the mediastinal pressure rises abruptly or if decompression via these routes is not sufficient, the mediastinal parietal pleura may rupture, resulting in pneumothorax. Entry of gas into the pulmonary circulation may produce systemic air embolism.⁹⁴ Even pneumoscrotum has been described as an unusual complication of barotrauma.⁹⁵ Pneumomediastinum can produce several interesting radiographic signs such as pneumopericardium, continuous diaphragm sign, continuous left hemidiaphragm sign, Naclerio's sign, V sign at confluence of brachiocephalic veins, thymic spinnaker-sail sign, ring-round-the-artery sign, and extrapleural sign.⁹⁶

Figure 48-2.

Infant with respiratory distress syndrome. The radiograph shows cysts and linear streaks of air, pneumopericardium, pneumoperitoneum, and subcutaneous emphysema. Although the radiograph belongs to an infant, it illustrates well the features of early barotrauma and its late complications.

Previous studies had shown that the factors that predispose to barotrauma are high peak and mean airway pressures, positive end-expiratory pressure (PEEP), use of volume-cycled ventilators, intubation of the right bronchus, chronic airways obstruction, and aspiration pneumonia.97, 98, 99, 100 However, some studies101, 102 have shown that the incidence of barotrauma is independent of airway pressure. Experts now accept that pulmonary edema and lung injury during mechanical ventilation are the consequence of “volutrauma” rather than “barotrauma.”¹⁰³ The best treatment for barotrauma is early recognition, and prevention-delayed treatment has a mortality of 31%.⁹⁷ The recommended preventive measures are to decrease peak airway pressure by decreasing tidal volume, peak flow, and ventilatory rate; to use the best PEEP; and to employ assist-control mode, independent lung ventilation, and high-frequency positive pressure ventilation.¹⁰⁰ In a study published by the Acute Respiratory Distress Syndrome Network, it was found that treatment with a ventilator strategy designed to protect the lungs from excessive stretch resulted in decreased mortality and increased the number of days without ventilator use in patients with acute lung injury and acute respiratory distress syndrome.¹⁰⁴

Pneumothorax after Fiberoptic Bronchoscopy and Needle Biopsy of the Lung

After a literature review of more than 9000 procedures of fiberoptic bronchoscopy (FOB) with transbronchial biopsy, Milam and colleagues¹⁰⁵ found that the rate of pneumothorax was 1.9%. After analyzing their series of patients who had undergone FOB with transbronchial biopsy, Milam and colleagues,¹⁰⁵ Frazier and colleagues,¹⁰⁶ and Blasco and colleagues¹⁰⁷ concluded that an immediate postbronchoscopic chest radiograph rarely provides clinically useful information and that in FOB without transbronchial biopsy, an immediate postbronchoscopy radiograph is not necessary. In a study published in June 2006, Izbicki and colleagues¹⁰⁸ also concluded that in asymptomatic patients, routine radiograph after transbronchial biopsy is not necessary. When biopsies are performed, the following groups of patients should be considered for postbronchoscopy radiograph: 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. Similarly, the complication of pneumothorax after transbronchial needle aspiration is also low (1 of 152 patients).¹⁰⁹

The incidence of pneumothorax after percutaneous needle biopsy110, 111, 112, 113 is much higher and ranges from 17% to 43%. Although some authors have found that a more central location of the lesion, COPD, and lung hyperinflation increase the risk of pneumothorax,114, 115 others found no correlation between development of pneumothorax and spirometric parameters or the presence of obstructive airways disease.111, 116 However, Kazerooni and others¹¹⁷ found that in patients with emphysema, there is a high incidence of pneumothorax after transthoracic needle aspiration; there is rapid development of pneumothorax in these cases, requiring chest tube placement. Delayed pneumothorax after percutaneous fine needle aspiration, although extremely unusual, has been reported in two cases and patients should be warned of this possible complication.¹¹⁸ More recently, Choi and colleagues¹¹⁹ reported on their series of 458 patients who had undergone transthoracic needle biopsy (TTNB). A follow-up chest radiograph was obtained immediately and 3 hours, 8 hours, 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

The reported incidence of pneumothorax after thoracentesis ranges from 5.7% to 19.2%.120, 121, 122, 123, 124 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 pressures develop.¹²⁵ Raptopoulos and colleagues¹²⁶ found that ultrasonographically guided thoracentesis, use of the smallest possible needle, and aspiration of the smallest possible amount of fluid are complicated by pneumothorax significantly less often than thoracentesis done with conventional techniques. Age, sex, underlying lung condition, overall clinical condition, size of the effusion, and type of tap (diagnostic or therapeutic) had no significant effect on the occurrence of pneumothorax after thoracentesis. In a recent review article, Feller-Kopman¹²⁷ concluded that the use of ultrasound for thoracentesis has been associated with improved yield and reduced complication rate and is quickly becoming the standard of care for procedural guidance.

Colt and colleagues,¹²⁸ reporting on 255 thoracenteses performed in 205 adult patients, found that hospitalization status, critical illness, effusion size or type, presence of loculations, operator, needle type, amount of fluid withdrawn, occurrence of dry tap, and type of thoracentesis were not associated with increased frequency of pneumothorax. The only predictor showing significant correlation was repeated thoracentesis. After an analysis of 506 thoracenteses in 370 patients, Aleman and colleagues¹²⁹ concluded that, in asymptomatic patients, the risk of developing pneumothorax was so low that the practice of obtaining a routine chest radiograph may not be justified. Chakrabarti and colleagues¹³⁰ reported the use of blind percutaneous pleural biopsy by Abrams needle in 75 patients; pneumothorax was seen in eight patients (11%), with only two patients requiring specific intervention.

Pneumothorax Resulting from Nasogastric Feeding Tubes

In 1978 James¹³¹ first reported pneumothorax as a complication of passing a narrow-bore nasogastric tube. Since that time numerous authors132, 133, 134, 135, 136, 137, 138, 139 have reported this complication.

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—all of which permit their undetected entry into the tracheobronchial tree, perforation of pulmonary tissue, and lodging in the pleural cavity.¹³⁴ Other factors associated with increased 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.¹³⁷ The clinical signs commonly used to ascer-tain 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.¹³³ 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 enteral feeding solution from the pleural space, mistaken for gastric contents, has been reported.¹³²

Pneumothorax after Percutaneous Dilational Tracheostomy

Percutaneous tracheostomy was first described in 1955. In 1985, Ciaglia and colleagues¹⁴⁰ described percutaneous dilational tracheostomy (PDT). Fikkers and colleagues¹⁴¹ described cases of subcutaneous emphysema and pneumothorax after percutaneous tracheostomy in a series of 326 cases. They described 7 of their own cases which had developed complications to include subcutaneous emphysema, mediastinal emphysema, and pneumothorax. Their review of literature showed that the incidence of subcutaneous emphysema was 1.4% and that of pneumothorax 0.8%. Findings associated with PTX included difficult PDT and the use of a fenestrated cannula.

Special Situations

Pneumothorax Ex Vacuo

Development of air in the pleural space after partial resolution of total bronchial obstruction,¹⁴² as a complication of lobar collapse,¹⁴³ and after therapeutic thoracentesis for malignant effusions¹⁴⁴ 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 endobronchial 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.¹⁴⁵

Sports-Related Pneumothorax

Experts have recognized that sports-related air leaks and pneumothorax occur more frequently than the literature suggests. Levy and colleagues¹⁴⁶ and Patridge and colleagues¹⁴⁷ each described three cases of pneumothorax or pneumomediastinum caused by blunt trauma sustained during a contact sport. Kizer and colleagues¹⁴⁸ identified 20 patients who had sustained a spontaneous or traumatic air leak while engaged in an outdoor sport.

Barotrauma Unrelated to Mechanical Ventilation

Although traditionally the term barotrauma has been used to describe development of extra alveolar air in a patient on mechanical ventilation, there are other situations in which, because of increased intraalveolar pressure, air leaks out of alveoli. Pulmonary barotrauma (PBT) of ascent is a well-known complication of compressed air diving. Tetzlaff and colleagues¹⁴⁹ found that preexisting small lung cysts or end-expiratory flow limitation may increase the risk of PBT, although Neuman and colleagues¹⁵⁰ contested these conclusions. Some experts have suggested that even minor forms of PBT should be considered a contraindication to further diving because the divers are prone to recurrences that can occur even at shallow depths.¹⁵¹ Clinically significant PBT has been reported from self-inflating bag-valve devices,¹⁵² after inflation of party balloons,¹⁵³ as a result of blast injury,154, 155 during submarine escape training,¹⁵⁶ after automobile air bag deployment,¹⁵⁷ and in a normal healthy volunteer after repeated measurements of maximal respiratory pressure.¹⁵⁸

CLINICAL FEATURES

The clinical features of pneumothorax depend on its size, the underlying lung condition, and whether the pneumothorax is tension in type. PSP usually develops in tall, thin males while the patients are at rest. Most often the onset of symptoms is not related to physical exertion. Surprisingly, many patients do not seek medical attention immediately after developing symptoms. In one series,¹⁵⁹ 18% of patients waited for more than 1 week after developing symptoms. Chest pain and dyspnea are the two main symptoms associated with the development of pneumothorax. In one series of 39 patients, all patients had one of the two symptoms and 25 of 39 patients (64%) had both.¹⁶⁰ The chest pain is sudden in onset; pleuritic in nature initially; and then becomes a persistent dull ache, localized to the affected site. The degree of dyspnea depends on the size of the pneumothorax and the condition of the underlying lung. Cough, malaise, orthopnea, or hemoptysis may be the presenting symptoms.

Small pneumothoraces (<25%) may not be detectable clinically, especially in a patient with emphysema. Larger pneumothorax may produce tachycardia and tachypnea. Decreased motion, vocal resonance, and breath sounds on the side of pneumothorax; hyperinflation; and hyperresonance usually exist. Pleural friction rub may be present. In a large pneumothorax, the trachea and apex beat may be shifted to the opposite side and liver dullness may be masked. The presentation in tension pneumothorax is more dramatic. Because of a ball-valve mechanism, air enters the pleural cavity but cannot escape, thereby building up positive pressure. As the tension continues to increase, the diaphragm is flattened, the mediastinum is shifted to the opposite side, and ultimately cardiopulmonary collapse results. In left-sided pneumothorax and in pneumomediastinum, systolic clicks, crunching, and whooping sounds have been described.161, 162, 163

Various unusual presentations and physical signs of pneumothorax have been described. Horner's syndrome may occur and is attributed to traction on sympathetic ganglion, secondary to mediastinal shift in tension pneumothorax.164, 165 Unilateral periorbital emphysema resembling ptosis was reported by Widder in two obtunded, cachectic patients.¹⁶⁶ The presence of undue resonance obtained by digital percussion on the medial zone of the clavicle with the patient in the orthostatic position has been described as an early and sole sign of pneumothorax.¹⁶⁷

The clinical features of pneumothorax in certain situations may not be typical, and the diagnosis is made by having a high index of suspicion. During a transbronchial biopsy a patient may complain of pleuritic pain, followed by progressive dyspnea. After subclavian vein catheterization, progressive dyspnea or alteration in the vital signs should alert the clinician to this complication. In a mechanically ventilated patient, development of pneumothorax can be suspected by new-onset respiratory distress, hypotension, agitation, unilateral decrease in breath sounds, worsening oxygenation, and a decrease in static and dynamic compliance.42, 168, 169 In sports-related pneumothorax, the presentation may be atypical, and pneumothorax may be difficult to recognize because an athlete's physical fitness may mask the serious injury and athletes may be more inclined to downplay their symptoms.¹⁴⁸

Simultaneous bilateral pneumothoraces is a rare and interesting condition. In humans, the right and left pleural spaces are completely separated. Theoretically, any patient who has undergone a median sternotomy, mediastinal surgery, heart or heart-lung transplant surgery is at risk for having a persistent pleuro-pleural channel. Most pleural rents probably heal but rarely a pleuro-pleural channel persists. Schorlemmer and colleagues¹⁷⁰ have referred to this condition as “iatrogenic buffalo chest” because the North American buffalo is one of few mammals that have communicating pleural spaces. A unilateral thoracic procedure in this situation has been described to cause bilateral pneumothoraces171, 172 and “shifting pneumothorax.”¹⁷³ Johri and colleagues¹⁷⁴ reported a patient who had undergone a thymoma resection in the remote past and developed bilateral pneumothoraces after undergoing transthoracic needle biopsy of a right lung nodule. Sayar and colleagues¹⁷⁵ described 12 patients who presented with simultaneous bilateral spontaneous pneumothorax (SBSP). They represented 1% of all patients with pneumothorax. Of the 12 patients, 5 (42%) had no underlying lung disease. In seven patients, SBSP was secondary to pulmonary metastases, histiocytosis, undefined interstitial pulmonary disease, tuberculosis, pneumonia, and chronic obstructive pulmonary disease.

The presence of pneumothorax may produce electrocardiographic changes suggesting myocardial ischemia or infarction. 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.176, 177, 178 The absence of ST-segment elevation and a significant Q-wave and reversal of electrocardiographic changes in the sitting position suggest pneumothorax. Most of these changes have been described in left-sided pneumothorax. Alikhan and Biddison¹⁷⁹ have described a new ECG sign of right-sided pneumothorax: loss of S-wave in lead V₂ and prominent R-wave voltage, which may mimic posterior wall myocardial infarction. Strizik and Forman¹⁸⁰ found PR-segment elevation in inferior leads and reciprocal PR-segment depression in an aVR lead in a case of left tension pneumothorax and attributed these to atrial ischemia or injury.

RADIOGRAPHIC SIGNS

The chest radiograph confirms the presence of pneumothorax in most cases. The air in the pleural space rises to the apex of the hemithorax and causes relaxation atelectasis of the upper portion of the lung. Classically, the clinician finds a visceral pleural line with absence of lung markings peripheral to this line. When the film cartridge used for the portable chest film is placed under the patient, the skin on the back can fold over on itself to produce a line that runs down the hemithorax, which can easily be mistaken for pneumothorax (Fig. 48-3 ). This line, pro duced by the redundant skinfold, can be differentiated from the line of pneumothorax by the following three features: (1) the lung markings are present peripheral to the skinfold; (2) the skinfold has a wavy appearance; and (3) in the skinfold, there is a gradual increase in radiodensity as the line is approached from the hilum. However, in the presence of a consolidated lung, a pneumothorax presents as an edge instead of a line.¹⁸¹

Figure 48-3.

Skinfold mimicking the pleural line of pneumothorax.

When pneumothorax is strongly suspected clinically but a pleural line is not clearly seen, possibly because of an overlying rib, gas in the pleural space can be detected by either of two procedures: (1) radiography in the erect posture (potentially more diagnostic with full expiration) or (2) radiography in the lateral decubitus position with a horizontal x-ray beam. Some authors,182, 183, 184 however, have suggested that the expiratory film does not increase diagnostic capability.

The diagnosis of pneumothorax in the critically ill patient is more difficult to establish. The following four variables occur statistically more often in patients with initial failure to diagnose pneumothorax: mechanical ventilation, atypical radiographic location of pneumothorax, altered mental status, and development of pneumothorax after peak physician staffing hours.¹⁸⁵

In the ICU setting, radiographs are typically obtained in the supine position, making pneumothorax diagnosis more difficult. In the supine position the gas within the pleural space rises to the highest point in the hemithorax, which, in this position, is the anterior costophrenic sulcus. Various authors have described the depression and clear visualization of the diaphragm anteriorly, creating a “double” appearance to the diaphragm, a deep lateral costophrenic angle on the involved side (“the deep sulcus sign”) (Fig. 48-4 ), an unusually distinct cardiac apex and pericardial fat tags, and increased hyperlucency of the upper abdominal quadrants.186, 187, 188, 189, 190 A sharp line outlining the descending aorta may be produced by air trapped behind the inferior pulmonary ligament. Any of these findings should lead to a prompt cross-table lateral or decubitus study or a CT scan to establish the diagnosis of pneumothorax.

Figure 48-4.

The deep sulcus sign in a supine patient.

Although not done commonly for the diagnosis of pneumothorax, CT of the chest may detect an unsuspected pneumothorax in a critically ill patient (Fig. 48-5 ).¹⁹¹ In view of the difficulty of clinically diagnosing pneumothorax in critically ill patients, Hall and colleagues¹⁹² have recommended daily chest radiographs for this group of patients. In those patients who are treated with PEEP, interstitial gas may be seen as an early sign of barotrauma: More than 50% of these go on to develop features of barotrauma.⁹² The interstitial gas is manifested radiographically by cystic changes, linear streaks along the bronchi and vessels, halos of gas around vessels, and subpleural gas. CT scan may also be useful to detect pneumothorax in complex cystic lung diseases.¹⁹³

Figure 48-5.

Computed tomography scan of chest showing pneumothorax.

Ultrasound examination is not used in the routine diagnosis of pneumothorax but may be of diagnostic utility. During the ultrasound examination, a kind of back-and-forth movement of lung (“lung sliding”), synchronized with respiration, is normally seen. Lichtenstein and Menu¹⁹⁴ found that absence of lung sliding was suggestive of pneumothorax. In a normal subject, in vertical orientation, the ultrasound screen shows artifacts rising from the pleural line and spreading to the edge of the screen (“comet-tail” artifacts). Lichtenstein and colleagues,¹⁹⁵ in a more recent report, concluded that ultrasound detection of “comet-tail” artifact at the anterior wall allows complete pneumothorax to be excluded.

MANAGEMENT

The goals of management of pneumothorax are (1) to rid the pleural space of air and allow reexpansion of the lung with the least possible morbidity and (2) to decrease the likelihood of recurrence. Approaches for the management of the initial episode include observation, supplemental oxygen, simple aspiration of the pneumothorax, or tube thoracostomy. The choice of therapy in a given patient depends on various factors such as the size of pneumothorax, whether the pneumothorax is primary or secondary, the condition of the lungs, the clinical stability of the patient, the occupation of the patient, and whether the pneumothorax has occurred in a special setting. For prevention of recurrence, chest tube placement with pleurodesis or various surgical interventions including thoracotomy or video-assisted thoracic surgery (VATS) may be necessary. However, as a postal survey of 3000 American College of Chest Physicians (ACCP) members showed, there exists marked practice variation in the clinicians' approaches to the management of spontaneous pneumothorax and bronchopleural fistula. This was partially explained by differences between pulmonologists and thoracic surgeons.¹⁹⁶ Many new recommendations that suggest a shift from the previous practices have been made and are discussed later.¹⁹⁷

Management of the First Episode of Pneumothorax

Estimating Size of Pneumothorax

A number of methods have been described to measure the size of pneumothorax.198, 199, 200 Engdahl and colleagues²⁰¹ found that the size of pneumothorax measured from a chest radiograph did not correlate with CT, whereas the size of pneumothorax as estimated by CT correlated well with the amount of air aspirated in 12 of 16 patients treated with drainage. They suggested that the decision to treat should be based on clinical status and, if it is considered important to determine the size, CT should be used.

Various approaches to the management of pneumothorax are discussed in subsequent sections.

Expectant Therapy

An estimated 1.25% of the volume of pneumothorax is absorbed each 24 hours. Therefore if a patient has a 20% pneumothorax, it will take 16 days for the air to be absorbed spontaneously. Different authors have used different sizes of pneumothorax in recommending expectant management: less than 15%,¹⁹⁹ less than 25%,56, 76 or an apical collapse of less than 4 cm and lateral collapse of less than 1 cm.²⁰²

The absorption of gas from the pleural space depends, besides other factors, on the gradient between the partial pressure in the capillaries and 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.¹⁹⁹ Studies203, 204 have shown that administering 100% oxygen increases absorption of air fourfold to sixfold. 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.¹⁹⁹

Removal of Air from Pleural Space

In those patients whose pneumothorax is large (more than 20% to 25%), progressive, or tension type; who are symptomatic; have an underlying chronic lung disease; are on a ventilator; or who have a recurrent pneumothorax, the pleural space air needs to be removed by various therapeutic means rather than be allowed to be absorbed spontaneously. The following methods have been used for the removal of air.

Simple Aspiration

Inserting an intercostal tube is a traumatic, painful procedure associated with a risk of hemorrhage. If connected to an underwater seal, the tube confines the patient to bed, thereby increasing the risk of thromboembolism and prolonging the duration of hospitalization. In view of these disadvantages, some investigators have treated pneumothorax by simple aspiration.205, 206, 207, 208 Simple aspiration is usually performed in the second intercostal space in the midclavicular line. The catheter is connected to a three-way tap with the exit tube placed under water to ensure correct direction of airflow. Resistance is felt as the reexpanded lung impinges on the cannula. A confirmatory chest radiograph is performed.

A large tension pneumothorax needs to be evacuated immediately. Thoracocentesis using a catheter (e.g., Seldinger technique) that is advanced into the pleural cavity by means of a metal needle, a butterfly needle, or a regular disposable needle is fraught with danger because the lung may be punctured. Wung and colleagues²⁰⁹ have described the use of a spring-loaded Veress needle (American Cystoscope Makers, Inc., Stamford, Conn.) for emergency thoracentesis. This needle consists of a slender spring-loaded inner tube, which is blunt tipped and has a side aperture, enclosed in a 16-gauge sharp needle. The spring action allows the inner needle to retract while the outer needle is puncturing the chest wall but lets it spring out as soon as the pleural cavity is punctured.

Simple aspiration is a technique with low morbidity that is well tolerated and allows the patient to be mobile and return to work rapidly. It may be used as the initial procedure in the absence of signs of tension.²¹⁰ Unfortunately, simple aspiration leaves the patient with a 10% to 50% chance of recurrence.159, 204, 205, 206 However, in a recent randomized, prospective, multicenter pilot study involving 60 patients with the first episode of PSP, Noppen and colleagues²¹¹ reported that manual aspiration seemed equally effective as chest tube drainage and was safe, well tolerated, and feasible as an outpatient procedure in the majority of patients. Devanand and colleagues,²¹² after a meta-analysis of three randomized controlled trials (RCTs) with a combined total of 194 patients, concluded that simple aspiration is advantageous in the initial management of PSP because of shorter hospitalization. No significant difference in recurrence was reported at 1 year using either modality, but the efficacy data were inconclusive.

Tube Thoracostomy

Modern chest tubes are made of clear plastic with varying internal diameters, multiple holes and distance markers, and radiopaque stripes that outline the proximal drainage hole. They are pliable but not supple enough to kink.

The second intercostal space in the midclavicular line is generally chosen for insertion of the tube because the area is wide and avascular. The tube is inserted using the trocar or blunt dissection method. Most institutions now prefer the latter. After insertion the tube is directed anteroapically and secured to prevent accidental removal. The tube is then connected to a water-seal drainage or a drainage system.²¹³ To avoid the risk of reexpansion pulmonary edema, it is recommended that negative suction not be applied in the absence of a bronchopleural fistula.²¹⁴

Bell and colleagues,²¹⁵ in 102 chest tube removals in 69 trauma patients, found that the post–chest tube removal pneumothoraces rates did not differ whether the chest tube was removed at end-expiration or end-inspiration. In the absence of trauma and with good aseptic technique, prophylactic antibiotics are not recommended.

The complications associated with thoracostomy that have been reported in the literature include laceration of the lung, spleen, liver, and stomach; intercostal artery bleeding; infarction of a peripheral segment of the lung aspirated into the drainage part of the chest tube; and delayed pulmonary perforation and subcutaneous emphysema.213, 216 A blocked tube may result in a residual pleural space with the development of empyema.²¹⁷

Percutaneous Pneumothorax Catheter

A number of authors218, 219 have described the use of small lumen catheters for treating a simple pneumothorax. In view of the ease of insertion, good response, and low incidence of complications, it has been suggested that a small lumen catheter may be a useful alternative to tube thoracotomy. Although catheter failure included kinking, malposition, inadvertent removal by the patient, occlusion of the tube or valve by pleural fluid, and large air leak, no complication attributable to tube placement occurred.²¹⁸ Liu and colleagues²²⁰ reported their experience with the use of pigtail catheters in 50 patients versus traditional chest tube in 52 patients and found that the pigtail drainage was no less effective than the traditional chest tube.

The questions pertaining to chest tubes such as small-bore tube versus large-bore tube, whether to apply suction or not, and whether the tube should be taken out at the end of inspiration or expiration have been discussed nicely by Baumann should be¹⁵ in a review article in 2006. These points are summarized in the management algorithms given later.

Thoracic Vent

Samelson and colleagues²²¹ and Martin and colleagues²²² have described their experiences with the thoracic vent (one-way valve feature) in managing simple pneumothorax. The thoracic vent is inserted in the second intercostal space in the midclavicular line. The authors point out that this device has the advantage of a urethane tube that does not kink, a self-contained one-way valve, and a unique signal diaphragm that reflects pleural pressure; however, the device is not suitable for use in patients who are expected to have large-volume or protracted air leaks.

Prevention of Recurrence

As mentioned earlier, the initial episode of spontaneous pneumothorax may be managed by simple observation or drainage. Once the initial episode of pneumothorax has resolved, the decision as to the need for measures to prevent recurrence must be made. In the following groups of patients, further management needs to be planned after the resolution of pneumothorax: recurrent pneumothorax, patients with chronic air leak, patients with demonstrable large bullae, and patients who live in remote areas or pursue an occupation in which a recurrence could be a hazard (e.g., airline personnel or divers).

Different recurrence rates have been reported by various authors and range from 20% to 52%.1, 202, 223, 224 The following are established risk factors for recurrence: more than one previous episode, COPD, air leak for more than 48 hours during the 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. The following approaches have been used.

Chemical pleurodesis via chest tube, at thoracotomy, or VATS can be used to institute preventive measures.

Chemical Sclerosis (Pleurodesis)

Pleurodesis (adhesion of visceral and parietal pleura) can be done by introducing the sclerotic agent via a chest tube, or it can be done in the operating room with open thoracotomy or thorascopy. However, there is no consensus about the timing or method of pleurodesis.²²⁵ A practical approach is outlined later in the management algorithm.

Because sterile tetracycline is no longer available, intrapleural instillation of doxycycline has been used as an alternative for pleurodesis.²²⁶ Talc, finely powdered magnesium silicate, is another effective pleural irritant, producing fibrosis and adhesions. Numerous complications and side effects such as fever, pain, infection, and respiratory failure have been reported with its use,²²⁷ but Lange and colleagues²²⁸ found that although talc may result in mild restrictive respiratory impairment in long-term follow-up, it was not clinically significant and there were no recorded cases of mesothelioma.

In the past, patients with failed pleurodesis underwent surgical intervention. Thoracic surgery in such patients is complicated by partial pleural symphysis. Also, previous chemical pleurodesis makes lung transplantation more difficult technically. In view of these concerns, Kirby and Ginsberg⁷⁶ recommend that chemical pleurodesis be used only in selected patients who are too ill for surgery.

Surgery

The objectives of surgical treatment are to obtain full reexpansion of the affected lung, control complications, tackle the underlying lung problem, and prevent recurrence through pleural sclerosis by mechanical abrasion or pleurectomy.

Indications

Surgical management during the first episode of SP 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 in these patients to control the bleeding; a trapped lung may fail to reexpand, and decortication is required in such cases. If the patient is a diver, airline pilot, or lives in a remote area, surgery should be considered after the first episode to prevent a recurrence.

Surgical Approach

Apical bullous disease can be surgically approached by a transaxillary approach76, 229 or through the auscultation triangle.²³⁰ In a young female, a cosmetically acceptable scar is produced by a submammary anterolateral incision.²¹⁰ In an older individual with difficult pneumothorax complicated by other problems, a formal posterolateral thoracotomy is recommended.76, 210, 229 If bilateral pleurectomy is required, a midline sternotomy is preferred. This permits access to both pleural cavities with minimum interference with respiratory function and causes minimal postoperative pain.²¹⁰

Surgical Techniques

Sites of air leaks and obvious bullae are oversewn.²²⁹ With modern stapling instruments, blebs and bullae can be excised easily with an airtight seal, without sacrificing a great amount of normal underlying lung tissue.⁷⁶ If one large cyst is fed by a major bronchial branch, then control of the feeding bronchus and marsupialization or plication of the bulla is performed. Segmentectomy and lobectomy to deal with underlying pathology are rarely necessary.²¹⁰

Obliteration of pleural space can be achieved by abrasion of the pleura with a dry gauze sponge, apical pleurectomy,²¹⁰ or an extensive pleurectomy.²³¹ When bilateral pleurectomy is advisable, it should be done in stages, 10 to 30 days apart. In most of the cases, blebectomy and pleural abrasion are sufficient.

In their study, Murray and colleagues²³² suggested an entirely different approach to the problem of recurrent pneumothorax. They used a limited axillary thoracotomy as primary treatment for recurrent pneumothorax, without a preoperative chest tube.

Thoracoscopic Surgery

Modern thoracoscopy allows minimally invasive access to the chest cavity. It allows full visualization of the lung and pleura and, when combined with resection of blebs and pleurodesis or pleurectomy, results in a low recurrence rate, minimal patient discomfort, and rapid recovery. Identified bullae can be treated with a variety of modalities.233, 234, 235 Chemical or mechanical pleurodesis can be performed during VATS.236, 237, 238 Thoracoscopic identification and treatment of bronchopleural fistulas are also possible in patients with prolonged air leaks despite chest tube drainage.²³⁹ Bilateral VATS has been found to be a safe and efficacious procedure for patients with bilateral bullous disease and patients presenting with simultaneous or nonsimultaneous bilateral SP.240, 241

Management under Special Circumstances

Pneumothorax in AIDS Patients

Pneumocystis jerovici pneumonia–related pneumothorax is complicated by a virulent form of necrotizing subpleural lesions, which result in diffuse air leaks that are refractory to the standard treatment.52, 57 Asymptomatic patients can be observed. An aggressive stepped-care management with large-bore intercostal tube drainage, chemical pleurodesis, and early video-assisted thoracic talc poudrage has been recommended for symptomatic patients.²⁴² In patients with an air leak persisting for more than 7 days, thoracotomy with stapling of blebs and mechanical pleurodesis has been recommended. When chemical pleurodesis is unsuccessful and open surgical pleurectomy is not desirable because of the patient's underlying disease, morbidity, and poor prognosis, thoracoscopic pleural ablation offers a therapeutic alternative.²³⁹

Pneumothorax in Cystic Fibrosis

Pleurodesis as an initial step in the management of pneumothorax in cystic fibrosis is considered contraindicated because it results in extensive pleural adhesions that jeopardize subsequent lung transplantation.²⁴³ Therefore Noyes and Orenstein²⁴⁴ have recommended a stepwise management of pneumothorax in cystic fibrosis. If initial tube thoracostomy does not bring resolution of air leak within 5 days, blebectomy should be performed. If blebectomy proves unsuccessful, with either continuing air leak or recurrence, a definitive pleural ablative procedure should be undertaken.

Catamenial Pneumothorax and Pneumothorax Complicating Pregnancy

The initial episode of catamenial pneumothorax is managed in the usual manner. Recurrences, which occur 72 hours before or after menstrual flow, are managed by pleurodesis or hormonal treatment.²⁴⁵ Therapeutic options include oral contraceptive pills, danazol, progestational agents, and gonadotropin-releasing hormone (GnRH) analogues.⁷² 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. At thoracotomy, any diaphragmatic defects should be closed, any subpleural blebs should be oversewn, and pleural abrasion should be performed to effect a pleurodesis.246, 247 A patient who has a previous or current catamenial pneumothorax is at increased risk for barotrauma with positive pressure ventilation and represents a unique challenge to the anesthetist. Postoperative hormonal therapy is often required to prevent recurrences. Hysterectomy or tubal ligation may benefit selected patients.⁷² Pneumothorax complicating pregnancy is managed in the usual way, but in view of the high rate of recurrence of pneumothorax during parturition, thoracotomy with resection of apical blebs (if present) should be considered.²⁴⁸

Pneumothorax in Air Travelers

Air or gas trapped in body cavities expands in direct proportion to the decrease in atmospheric pressure. At an altitude of 10,000 feet, a pneumothorax will increase 1.5 times in size.²⁴⁹ If a patient with pneumothorax, especially secondary to COPD, has to be transported, the following precautions should be taken: (a) the ability of the patient to take supplemental oxygen without causing alveolar hypoventilation must be established before the flight and supplemental oxygen administered during the flight; (b) a chest tube with a Heimlich flutter valve should be in place; and (c) the patient should travel with a medically knowledgeable companion.²⁵⁰

Management of Pneumothorax in Severe Acute Respiratory Syndrome

The 2002 epidemic of the severe acute respiratory syndrome (SARS) brought several ethical issues associated with new, severe epidemic diseases into sharp focus. Of the six cases described by Sihoe,²⁵¹ pneumothoraces were bilateral in three patients, mechanical ventilation was indicated in three patients, and two patients died. Air leaks or recurrences occurred in all four patients who accepted chest tubes. These air leaks took 14 to 31 days to resolve. Peripheral leukocytes and serum lactate dehydrogenase were higher in SARS patients with pneumothorax. These complications reflected severe pathologic changes in lung tissues and the strong pulmonary and systemic inflammatory responses that accompany SARS. During the SARS epidemic, health care providers were at risk, with substantial risk for those who performed bronchoscopy. By the end of the epidemic, approximately 30% of reported cases were in health care workers and some died. Felice²⁵² concluded that if multiple management options are available and they can be expected to result in equivalent, optimal patient outcomes, options that pose lesser risks to health care providers should be selected.

Management of Pneumothorax in Lymphangioleiomyomatosis

Lymphangioleiomyomatosis (LAM) is a rare and frequently fatal disease that exclusively affects women of childbearing age. Thin-walled cyst formation occurs in the pulmonary parenchyma, and lung function declines progressively. The LAM Pleural Disease Consensus Group reviewed the responses to a questionnaire by 395 patients. Of these, 260 patients (incidence, 66%) reported at least one spontaneous pneumothorax during their lifetime and 200 out of 260 (77%) indicated that they had subsequent pneumothoraces.²⁵³ Because of the morbidity and cost associated with multiple recurrences, the authors recommended early, definitive intervention, preferably at the time of the initial pneumothorax. Although pleurodesis may be associated with an increased risk of perioperative bleeding with lung transplantation, their data suggested that the complications are manageable and do not preclude successful transplantation.

Persistent Pulmonary Air Leak and Bronchopleural Fistula

A persistent pulmonary air leak, which may occur as a result of pneumothorax or after pulmonary resection, is a difficult and frustrating problem to manage. Conventionally, the air leak persisting for more than 7 days is called bronchopleural fistula and it is not an uncommon problem. In the series reported by Chee and colleagues,²⁵⁴ the overall incidence of bronchopleural fistula was 34.6%. In pulmonary resection cases, Cerfolio and colleagues,²⁵⁵ on univariate analysis, found that the increased age and the following findings on pulmonary function testing predicted air leak on postoperative day one: low forced expiratory volume in 1 second/forced vital capacity ratio (FEV₁/FVC), increased residual volume/total lung capacity ratio (RV/TLC), increased RV, and increased functional residual capacity (FRC). In the patients with air leaks who are managed by tube thoracostomy, Cerfolio and colleagues²⁵⁵ found that conversion from suction to a water seal is an effective way of sealing an expiratory air leak. If the leak persists beyond 7 days, tube thoracostomy is deemed to have failed and a more definitive treatment is planned. Such cases are usually managed surgically, but patients who are unfit or unwilling for surgery pose a management dilemma. Chemical pleurodesis may be tried but does not succeed if the lung has failed to expand. In such a situation, autologous “blood patch” pleurodesis has been found useful.256, 257 Kinoshita and colleagues²⁵⁸ have described a technique for such cases. They used a large amount of diluted fibrin glue for pleurodesis in patients with intractable pneumothorax or intrapleural dead space and found it useful. If pleurodesis also fails, the leak is localized during fiberoptic bronchoscopy and the fistula is sealed by using a sealant.²⁵⁹ Pectoral myoplasty, in which the right pectoralis major muscle was transferred into the thorax and draped over the area of lung with multiple leaks, has been used when other interventions fail.²⁶⁰ Murata and colleagues²⁶¹ have described a closure with intravenous administration of a coagulation factor XIII concentrate. Ferguson and colleagues²⁶² reported closure of a persistent distal bronchopleural fistula using a one-way endobronchial valve designed for the treatment of emphysema.

COMPLICATIONS RELATED TO MANAGEMENT

Ziskind and colleagues,²⁶³ in 1965, described a case of pneumothorax in which accidental application of high, negative intrapleural pressure led to acute pulmonary edema. Since that time, unilateral expansion pulmonary edema has been recognized as a complication that can occur during the management of pneumothorax (Fig. 48-6 ). Reexpansion pulmonary edema tends to occur with greater frequency in patients 20 to 39 years of age, when there is complete collapse of the lung, when the pneumothorax has remained untreated for more than 72 hours, and when rapid reexpansion occurs secondary to the application of negative pressure; age-related changes in the older patients seem to afford some protection.214, 264 The exact pathogenesis of reexpansion pulmonary edema is not known, but various factors such as bronchial obstruction,²⁶⁵ decrease in surfactant,²⁶⁶ and increased capillary permeability267, 268 have been implicated. The development of bilateral reexpansion pulmonary edema after unilateral pleurodesis in a young male without heart disease might suggest that forces leading to ipsilateral reexpansion pulmonary edema also affect the contralateral lung.²⁶⁹

Figure 48-6.

A, Large pneumothorax. B, Reexpansion pulmonary edema.

Pavlin and colleagues²⁷⁰ have described three cases of reexpansion hypotension that followed rapid evacuation of persistent unilateral pneumothorax. Besides the presence of pulmonary collapse for more than 3 days, the other risk factors were significant arterial hypoxemia during pneumothorax, an elevated or rising hemoglobin and hematocrit level, and development of respiratory distress after insertion of a pleural drain. The mechanism of hypotension and shock after pulmonary reexpansion is not clear, but volume depletion and myocardial depression possibly play a role.

Slow expansion by intermittent clamping of the chest tube, especially in high-risk patients, may prevent both reexpansion edema and reexpansion hypotension.214, 270 Paradoxically, vigorous fluid therapy may be advantageous in preserving circulation dynamics despite coexisting pulmonary edema. Myocardial stimulants may be useful if myocardial depression is suspected.²⁷⁰ Diuretics have been used to manage reexpansion pulmonary edema²¹⁴ but may prove dangerous in the presence of hypovolemia and shock.²⁷¹ It has been recommended that a more logical approach in patients with shock and hypoxemia may be to use mechanical ventilation with PEEP, which would reduce further fluid shift into the reexpanded lung. Plasma expanders, fluid replacement, and vasopressor therapy can be used as needed.270, 272

Development of tension pneumothorax has been reported after inadvertent, improper attachment of a Heimlich valve.273, 274

GUIDELINES FOR MANAGING PNEUMOTHORAX

A more aggressive approach to managing pneumothorax has been advocated recently.²⁷⁵ Guidelines for managing pneumothorax have been published.276, 277

• Pneumothorax size: American College of Chest Physician (ACCP) guidelines define a small pneumothorax as less than 3 cm in apex-to-cupola distance; British Thoracic Society (BTS) guidelines define a small pneumothorax as a visible rim of less than 2 cm between the lung margin and chest wall.

• Stable patient: The ACCP defines a stable patient as one who has all of the following: respiratory rate less than 24 breaths per minute; heart rate greater than 60 beats per minute or less than 120 beats per minute; normal blood pressure; room air saturation of greater than 90%; and ability to speak in whole sentences.

• Imaging of pneumothorax: Expiratory chest radiographs are not recommended for the routine diagnosis. A lateral view or a lateral decubitus film should be performed if the posteroanterior (PA) view is normal and the suspicion for pneumothorax is high. BTS guidelines recommend CT scan to differentiate a pneumothorax from complex lung disease, when aberrant tube placement is suspected, and when plain radiograph is obscured by surgical emphysema. The ACCP panel did not achieve consensus regarding the role of CT.

• Management of chest tubes: Some controversy exists regarding the size of the tube in various situations and the use of suction. According to BTS, there is no evidence that large tubes (20 to 24 French [Fr]) are any better than smaller tubes (10 to 14 Fr) in the management of pneumothorax. However, a small chest tube may need to be replaced by a larger tube if leaking persists and creates management difficulty.

A PRACTICAL APPROACH TO THE MANAGEMENT OF PNEUMOTHORAX

The clinician finds it most practical to use a “roadmap” in different clinical scenarios. The difference between didactic medicine and bedside medicine is that the former is taught in a classroom and begins with a “diagnosis”; the latter starts at the bedside with a clinical scenario as the starting point. Figure 48-7 represents an algorithmic approach to management that is based on the ACCP and BTS guidelines and practical experience. It can be applied to most patients with pneumothoraces.

Figure 48-7.

Algorithmic approach to the management of pneumothorax.

Acknowledgments

The authors thank Faroque Khan, MB, MACP, for valuable advice and for contributing most of the radiographs; Dvorah Balsam, MD, for Fig. 48-2; and Leonard Octavius Barrett, MD, FACS, Chief of Thoracic Surgery at NUMC, for his comments regarding the surgical therapy.

KEY POINTS.

• ▪PSP occurs primarily in tall, thin, previously healthy young men, most of whom are smokers. Chest radiograph often shows apical subpleural blebs or bullae. Rupture of these bullae is not related to physical activity but may be related to changes in atmospheric pressure. COPD is the most common cause of secondary pneumothorax. Presentation of pneumothorax in COPD is often atypical and causes excessive morbidity and mortality.
• ▪A high incidence of pneumothorax occurs in AIDS patients, related to PCP and the mechanical ventilation and bronchoscopy that are commonly required in these patients. In this group of patients, pneumothorax is frequently bilateral, recurrent, and unresponsive to conservative therapy.
• ▪Traumatic pneumothorax, which occurs as a result of a penetrating injury, may occur with closed chest trauma.
• ▪PTX is a common complication of mechanical ventilation. Interstitial emphysema is a harbinger of this complication. High peak and mean airway pressures, PEEP, use of volume-cycled ventilators, intubation of right mainstem bronchus, chronic airways obstruction, and aspiration pneumonia increase the incidence.
• ▪Pneumothorax ex vacuo, sports-related pneumothorax, and barotrauma unrelated to mechanical ventilation are interesting conditions that are not common, but they are important to be aware of.
• ▪Simultaneous bilateral pneumothoraces and “shifting pneumothoraces” are rare but interesting conditions and may develop because of persistent pleuro-pleural communication called iatrogenic buffalo chest.
• ▪An immediate postbronchoscopy chest radiograph is rarely useful but should be done in certain groups of patients (e.g., comatose, mentally retarded, ventilated, or with respiratory compromise).
• ▪PTX induced by a misplaced small-bore feeding tube is not uncommon. Clinical signs may be misleading.
• ▪A visceral pleural line with absence of lung markings peripherally is the classic radiographic sign of PTX. When the chest radiograph is obtained in the supine position, the signs are very different.
• ▪The approach to management of a PTX is dictated by the clinical condition rather than merely the size of the PTX, which is best estimated by CT scan of the chest. Expectant therapy is recommended for a small PSP in a stable patient. Reabsorption of air is hastened by 100% oxygen.
• ▪Air can be removed by simple aspiration, a small lumen catheter, or tube thoracostomy. Unstable patients with large secondary PTXs must be managed with tube thoracostomy.
• ▪A staged approach is recommended for chest tube removal. In PSP cases, the tube can be removed 6 to 12 hours after evidence of air leak was last seen; this waiting period is 12 to 24 hours in secondary PTX.
• ▪Definitive management of recurrent pneumothorax or persistent leak can be done by open thoracotomy or video-assisted thoracoscopy associated with pleurodesis, pleural abrasion, parietal pleurectomy, or bullectomy. In patients unsuitable or unwilling for surgery, chemical pleurodesis via a chest tube may be done.
• ▪PTX tends to recur in patients with cystic fibrosis. Blebectomy, without stripping the pleura, is recommended in these patients so that they may remain transplant candidates. Pleurodesis should not be done in these cases because adhesion development jeopardizes subsequent lung transplantation.
• ▪PTX in pregnancy is managed in the usual manner initially. In view of the high recurrence rates during parturition, thoracotomy with resection of blebs should be considered.
• ▪Reexpansion pulmonary edema is an important complication and can be prevented by slow expansion in high-risk patients.