- Author: Brian J Daley, MD, MBA, FACS, FCCP, CNSC; Chief Editor: Mary C Mancini, MD, PhD, MMM more...
Pneumothorax is defined as the presence of air or gas in the pleural cavity (ie, the potential space between the visceral and parietal pleura of the lung), which can impair oxygenation and/or ventilation. The clinical results are dependent on the degree of collapse of the lung on the affected side. If the pneumothorax is significant, it can cause a shift of the mediastinum and compromise hemodynamic stability. Air can enter the intrapleural space through a communication from the chest wall (ie, trauma) or through the lung parenchyma across the visceral pleura. See the image below.
Signs and symptoms
The presentation of patients with pneumothorax varies depending on the following types of pneumothorax and ranges from completely asymptomatic to life-threatening respiratory distress:
Spontaneous pneumothorax: No clinical signs or symptoms in primary spontaneous pneumothorax until a bleb ruptures and causes pneumothorax; typically, the result is acute onset of chest pain and shortness of breath, particularly with secondary spontaneous pneumothoraces
Iatrogenic pneumothorax: Symptoms similar to those of spontaneous pneumothorax, depending on patient’s age, presence of underlying lung disease, and extent of pneumothorax
Tension pneumothorax: Hypotension, hypoxia, chest pain, dyspnea
Catamenial pneumothorax: Women aged 30-40 years with onset of symptoms within 48 hours of menstruation, right-sided pneumothorax, and recurrence
Pneumomediastinum: Must be differentiated from spontaneous pneumothorax; patients may or may not have symptoms of chest pain, persistent cough, sore throat, dysphagia, shortness of breath, or nausea/vomiting
See Clinical Presentation for more detail.
History and physical examination remain the keys to making the diagnosis of pneumothorax. Examination of patients with this condition may reveal diaphoresis and cyanosis (in the case of tension pneumothorax). Affected patients may also reveal altered mental status changes, including decreased alertness and/or consciousness (a rare finding).
Findings on lung auscultation vary depending on the extent of the pneumothorax. Respiratory findings may include the following:
Respiratory distress (considered a universal finding) or respiratory arrest
Tachypnea (or bradypnea as a preterminal event)
Asymmetric lung expansion: Mediastinal and tracheal shift to contralateral side (large tension pneumothorax)
Distant or absent breath sounds: Unilaterally decreased/absent lung sounds common, but decreased air entry may be absent even in advanced state of pneumothorax
Minimal lung sounds transmitted from unaffected hemithorax with auscultation at midaxillary line
Hyperresonance on percussion: Rare finding; may be absent even in an advanced state
Decreased tactile fremitus
Adventitious lung sounds: Ipsilateral crackles, wheezes
Cardiovascular findings may include the following:
Tachycardia: Most common finding; if heart rate is faster than 135 beats/min, tension pneumothorax likely
Hypotension: Inconsistently present finding; although typically considered a key sign of tension pneumothorax, hypotension can be delayed until its appearance immediately precedes cardiovascular collapse
Jugular venous distention: Generally seen in tension pneumothorax; may be absent if hypotension is severe
Cardiac apical displacement: Rare finding
Common findings among the types of pneumothoraces include the following:
Spontaneous and iatrogenic pneumothorax: Tachycardia most common finding; tachypnea and hypoxia may be present
Tension pneumothorax: Variable findings; respiratory distress and chest pain; tachycardia; ipsilateral air entry on auscultation; breath sounds absent on affected hemithorax; trachea may deviate from affected side; thorax may be hyperresonant; jugular venous distention and/or abdominal distention may be present
Pneumomediastinum: Variable or absent findings; subcutaneous emphysema is the most consistent sign; Hamman sign—a precordial crunching noise synchronous with the heartbeat and often accentuated during expiration—has a variable rate of occurrence, with one series reporting 10%
Lab and imaging studies
Although laboratory and imaging studies help determine a diagnosis, tension pneumothorax primarily is a clinical diagnosis based on patient presentation. Suspicion of tension pneumothorax, especially in late stages, mandates immediate treatment and does not require potentially prolonged diagnostic studies.
Arterial blood gas (ABG) studies measure the degrees of acidemia, hypercarbia, and hypoxemia, the occurrence of which depends on the extent of cardiopulmonary compromise at the time of collection. ABG analysis does not replace physical diagnosis, nor should treatment be delayed while awaiting results if symptomatic pneumothorax is suspected. However, ABG analysis may be useful in evaluating hypoxia and hypercarbia and respiratory acidosis.
When pneumothorax is suspected, confirmation by chest radiography affords additional information beyond confirmation, such as the extent of pneumothorax, potential causes, a baseline study from which to go forward, and assistance with the therapeutic plan.
The following radiologic studies may be used to evaluate suspected pneumothorax:
Chest radiography: Anteroposterior and/or lateral decubitus films
Contrast-enhanced esophagography: If emesis/retching is the precipitating event
Chest computed tomography scanning: Most reliable imaging study for diagnosis of pneumothorax but not recommended for routine use in pneumothorax
See Workup for more detail.
Although there is general agreement on the management of pneumothorax, a full consensus about management of initial or recurrent pneumothorax does not exist. Rather, many clinicians use a risk stratification framework as well as other approaches for choosing among options to restore lung volume and an air-free pleural space and to prevent recurrences.
The range of medical therapeutic options for pneumothorax includes the following:
Watchful waiting, with or without supplemental oxygen
Tube drainage, with or without medical pleurodesis
If the patient has had repeated episodes of pneumothorax or if the lung remains unexpanded after 5 days with a chest tube in place, operative therapy such as the following may be necessary:
Thoracoscopy: Video-assisted thoracoscopic surgery (VATS)
Electrocautery: Pleurodesis or sclerotherapy
Resection of blebs or pleura
The following medications may be used to aid in the management of patients with pneumothorax:
Local anesthetics (eg, lidocaine hydrochloride)
Opioid anesthetics (eg, fentanyl citrate, morphine)
Benzodiazepines (eg, midazolam, lorazepam)
Antibiotics (eg, doxycycline, cefazolin)
See Treatment and Medication for more detail.
Pneumothorax is defined as the presence of air or gas in the pleural cavity (ie, the potential space between the visceral and parietal pleura of the lung). The clinical results are dependent on the degree of collapse of the lung on the affected side. Pneumothorax can impair oxygenation and/or ventilation. If the pneumothorax is significant, it can cause a shift of the mediastinum and compromise hemodynamic stability. Air can enter the intrapleural space through a communication from the chest wall (ie, trauma) or through the lung parenchyma across the visceral pleura.
Among the topics this article will discuss are several areas of new information in the medical literature: (1) studies comparing aspiration and tube drainage for treatment of primary spontaneous pneumothorax, (2) long-term follow-up of surgical treatment of pneumothorax, (3) assessment of the impact of pleurodesis on transplantation outcomes in patients with lymphangiomyomatosis, (4) demonstrated utility of ultrasonography in the bedside diagnosis of iatrogenic pneumothorax, and (5) inability of ultrasonography to distinguish between intrapulmonary bullae and pneumothorax.
See also Restoring an Air-Free Pleural Space in Pneumothorax.
Primary and secondary spontaneous pneumothorax
Spontaneous pneumothorax is a commonly encountered problem with approaches to treatment that vary from observation to aggressive intervention. Primary spontaneous pneumothorax (PSP) occurs in people without underlying lung disease and in the absence of an inciting event (see the images below). In other words, air enters into the intrapleural space without preceding trauma and without an underlying history of clinical lung disease. However, many patients whose condition is labeled as primary spontaneous pneumothorax have subclinical lung disease, such as pleural blebs, that can be detected by CT scanning. Patients are typically aged 18-40 years, tall, thin, and, often, are smokers.
Secondary spontaneous pneumothorax (SSP) occurs in people with a wide variety of parenchymal lung diseases. These individuals have underlying pulmonary pathology that alters normal lung structure (see the image below). Air enters the pleural space via distended, damaged, or compromised alveoli. The presentation of these patients may include more serious clinical symptoms and sequelae due to comorbid conditions.
Iatrogenic and traumatic pneumothorax
Iatrogenic pneumothorax is a traumatic pneumothorax that results from injury to the pleura, with air introduced into the pleural space secondary to diagnostic or therapeutic medical intervention (see the following image). Half a century ago, iatrogenic pneumothorax was predominantly the result of deliberate injection of air into the pleural space for the treatment of tuberculosis (TB). The terminology evolved to the preference for "induced" or "artificial" pneumothorax to indicate pulmonary TB treatment, before arriving at the current classification. Pulmonary TB remains a significant cause of secondary pneumothorax.
Traumatic pneumothorax results from blunt trauma or penetrating trauma that disrupts the parietal or visceral pleura (see the images below). Management steps for traumatic pneumothoraces are similar to those for other, nontraumatic causes. If hemodynamic or respiratory status is compromised or an open (communicating to the atmosphere) and/or hemothorax are also present, tube thoracostomy is performed to evacuate air and allow re-expansion of the lung. There is a subset of traumatic pneumothoraces classified as occult; that is, they cannot be seen on chest radiographs but can be seen on CT scans. In general, these can be observed and treated if they become symptomatic.
A tension pneumothorax is a life-threatening condition that develops when air is trapped in the pleural cavity under positive pressure, displacing mediastinal structures and compromising cardiopulmonary function. Prompt recognition of this condition is life saving, both outside the hospital and in a modern ICU. Because tension pneumothorax occurs infrequently and has a potentially devastating outcome, a high index of suspicion and knowledge of basic emergency thoracic decompression procedures are important for all healthcare personnel. Immediate decompression of the thorax is mandatory when tension pneumothorax is suspected. This should not be delayed for radiographic confirmation. Note the image below.
Pneumomediastinum is the presence of gas in the mediastinal tissues occurring spontaneously or following procedures or trauma (see the following images). A pneumothorax may occur secondary to pneumomediastinum.
The inner surface of the thoracic cage (parietal pleura) is contiguous with the outer surface of the lung (visceral pleura); this space contains a small amount of lubricating fluid and is normally under negative pressure compared to the alveoli. Determinants of pleural pressure are the opposing recoil forces of the lung and chest wall.
The underlying pathophysiology of pneumothorax is reviewed in this section.
Spontaneous pneumothorax in most patients occurs from the rupture of blebs and bullae. Although PSP is defined as occurring in patients without underlying pulmonary disease, these patients have asymptomatic blebs and bullae detected on computed tomography scans or during thoracotomy. PSP is typically observed in tall, young people without parenchymal lung disease and is thought to be related to increased shear forces in the apex.
Although PSP is associated with the presence of apical pleural blebs, the exact anatomic site of air leakage is often uncertain. Fluorescein-enhanced autofluorescence thoracoscopy (FEAT) is a novel method to examine the site of air leak in PSP. FEAT-positive lesions can be detected that appear normal when viewed under normal white-light thoracoscopy.
In normal respiration, the pleural space has a negative pressure. As the chest wall expands outward, the surface tension between the parietal and visceral pleura expands the lung outward. The lung tissue intrinsically has an elastic recoil, tending to collapse inwards. If the pleural space is invaded by gas from a ruptured bleb, the lung collapses until equilibrium is achieved or the rupture is sealed. As the pneumothorax enlarges, the lung becomes smaller. The main physiologic consequence of this process is a decrease in vital capacity and partial pressure of oxygen.
Lung inflammation and oxidative stress are hypothesized to be important to the pathogenesis of PSP. Current smokers, at increased risk for PSP, have increased numbers of inflammatory cells in the small airways. Bronchoalveolar lavage (BAL) studies in patients with PSP reveal that the degree of inflammation correlates with the extent of emphysematouslike changes (ELCs). One hypothesis is that ELCs result from degradation of lung tissue due to imbalances of enzymes and antioxidants released by innate immune cells. In one study, erythrocyte superoxide dismutase activity was significantly lower and plasma malondialdehyde levels higher in patients with PSP than in normal control subjects.
A growing body of evidence suggests that genetic factors may be important in the pathogenesis of many cases of PSP. Familial clustering of this condition has been reported. Genetic disorders that have been linked to PSP include Marfan syndrome, homocystinuria, and Birt-Hogg-Dube (BHD) syndrome.
Birt-Hogg-Dube syndrome is an autosomal dominant disorder that is characterized by benign skin tumors (hair follicle hamartomas), renal and colon cancer, and spontaneous pneumothorax. Spontaneous pneumothorax occurs in about 22% of patients with this syndrome. The gene responsible for this syndrome is a tumor suppressor gene located on band 17p11.2. The gene encoding folliculin (FLCN) is thought to be the etiology of Birt-Hogg-Dube syndrome. Multiple mutations have been found, and phenotypic variation is recognized. In one study, eight patients without skin or renal involvement had lung cysts and spontaneous pneumothorax. A germ-line mutation to this gene has been found in five patients, and genetic testing is now available.
Tension pneumothorax occurs anytime a disruption involves the visceral pleura, parietal pleura, or the tracheobronchial tree. This condition develops when injured tissue forms a one-way valve, allowing air inflow with inhalation into the pleural space and prohibiting air outflow. The volume of this nonabsorbable intrapleural air increases with each inspiration because of the one-way valve effect. As a result, pressure rises within the affected hemithorax. In addition to this mechanism, the positive pressure used with mechanical ventilation therapy can cause air trapping.
As the pressure increases, the ipsilateral lung collapses and causes hypoxia. Further pressure increases cause the mediastinum to shift toward the contralateral side and impinge on and compress both the contralateral lung and impair the venous return to the right atrium. Hypoxia results as the collapsed lung on the affected side and the compressed lung on the contralateral side compromise effective gas exchange. This hypoxia and decreased venous return caused by compression of the relatively thin walls of the atria impair cardiac function. Kinking of the inferior vena cava is thought to be the initial event restricting blood to the heart. It is most evident in trauma patients who are hypovolemic with reduced venous blood return to the heart.
Arising from numerous causes, this condition rapidly progresses to respiratory insufficiency, cardiovascular collapse, and, ultimately, death if unrecognized and untreated.
With pneumomediastinum, excessive intra-alveolar pressures lead to rupture of alveoli bordering the mediastinum. Air escapes into the surrounding connective tissue and dissects further into the mediastinum. Esophageal trauma or elevated airway pressures may also allow air to dissect into the mediastinum. Air may then travel superiorly into the visceral, retropharyngeal, and subcutaneous spaces of the neck. From the neck, the subcutaneous compartment is continuous throughout the body; thus, air can diffuse widely.
Mediastinal air can also pass inferiorly into the retroperitoneum and other extraperitoneal compartments. If the mediastinal pressure rises abruptly or if decompression is not sufficient, the mediastinal parietal pleura may rupture and cause a pneumothorax (in 10-18% of patients).
A wide variety of disease states and circumstances may result in a pneumothorax.
Primary and secondary spontaneous pneumothorax
Risks factors for primary spontaneous pneumothorax (PSP) include the following:
Tall, thin stature in a healthy person
Blebs and bullae (sometimes called referred to as ELCs) are related to the occurrence of primary spontaneous pneumothorax. Thoracic computed tomography (CT) scans of patients with PSP shows ipsilateral ELC in 89% and contralateral changes in 80% compared with a rate of 20% among control subjects matched for age and smoking. Nonsmokers with PSP had CT scan ELC abnormalities of 80% compared with a rate of 0% among nonsmoker controls without PSP.
Although patients with PSP do not have overt parenchymal disease, this condition is heavily associated with smoking—80-90% of PSP cases occur in smokers or former smokers, and the relative risk of PSP increases as the number of cigarettes smoked per day increases; that is, the risk of PSP is related to the intensity of smoking, with 102 times higher incidence rates in males who smoke heavily (ie, >22 cigarettes/day), compared with a sevenfold increase in males who smoke lightly (1-12 cigarettes/day). This incremental risk with increasing number of cigarettes smoked per day is much more pronounced in female smokers.
Typical PSP patients also tend to have a tall and thin body habitus. Whether height affects development of subpleural blebs or whether more negative apical pleural pressures cause preexisting blebs to rupture is unclear.
Pregnancy is an unrecognized risk factor, as suggested by a 10-year retrospective series in which five of 250 spontaneous pneumothorax cases were in pregnant women. The cases were all managed successfully with simple aspiration or video-assisted thoracoscopic surgery (VATS), and no harm occurred to mother or fetus.
Other associations with pneumothorax include increased intrathoracic pressure with the Valsalva maneuver, though contrary to popular belief, most spontaneous pneumothoraces occur while the patient is at rest. Changes in atmospheric pressure, proximity to loud music, and low-frequency noises are other reported factors.
Familial associations have been noted in more than 10% of patients. Some are due to rare connective tissue diseases, but mutations in the gene encoding folliculin (FLCN) have been described. These patients may represent an incomplete penetrance of an autosomal dominant genetic disorder. Birt-Hogg-Dube syndrome is characterized by benign skin growths, pulmonary cysts, and renal cancers and is caused by mutations in the FLCN gene.
In one family study, nine ascertained cases of spontaneous pneumothorax were reported among 54 members. A review of the literature summarized 61 reports of familial spontaneous pneumothorax among 22 families. Up to 10% patients with spontaneous pneumothorax report a positive family history.
Although rare, spontaneous pneumothorax occurring bilaterally and progressing to tension pneumothorax has been documented.
Diseases and conditions associated with secondary spontaneous pneumothorax include the following:
Chronic obstructive lung disease (COPD) or emphysema - Increased pulmonary pressure due to coughing with a bronchial plug of mucus or phlegm bronchial plug may play a role.
Human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) with PCP infection
Bronchogenic carcinoma or metastatic malignancy
Idiopathic pulmonary fibrosis
Inhalational and intravenous drug use (eg, marijuana, cocaine) 
Interstitial lung diseases associated with connective tissue diseases
Langerhans cell histiocytosis
Severe acute respiratory syndrome (SARS) - A reported 1.7% of SARS patients developed spontaneous pneumothorax. 
Thoracic endometriosis and catamenial pneumothorax
Collagen vascular disease, including Marfan syndrome
SSPs occur in the presence of lung disease, primarily in the presence of COPD. Other diseases that may be present when SSPs occur include tuberculosis, sarcoidosis, cystic fibrosis, malignancy, and idiopathic pulmonary fibrosis.
Pneumocystis jiroveci pneumonia (previously known as Pneumocystis carinii pneumonia [PCP]) was a common cause of SSP in patients with AIDS during the last decade. In fact, 77% of AIDS patients with spontaneous pneumothorax had thin-walled cavities, cysts, and pneumothorax from PCP infection. With the advent of highly active antiretroviral therapy (HAART) and widespread use of trimethoprim-sulfamethoxazole (TMP-SMZ) prophylaxis, the incidence of PCP and associated SSP has significantly declined.
PCP in other immunocompromised patients is seen only when TMP-SMZ prophylaxis is withdrawn prematurely. For practical purposes, if the immunocompromised patient has been taking TMP-SMZ prophylaxis reliably, PCP is reasonably excluded from the differential diagnosis and should not be a causative factor for SSP.
In cystic fibrosis, up to 18.9% of patients have been reported to develop spontaneous pneumothoraces, and they have a high incidence of recurrence on the same side after conservative management (50%) or intercostal drainage (55.2%). The risk of SSP in these patients increases with Burkholderia cepacia or Pseudomonas infections and allergic bronchopulmonary aspergillosis (ABPA). Pleurodesis increases the risk of bleeding associated with lung transplantation but is not an absolute contraindication.
Many different types of malignancies are known to present with a pneumothorax, especially sarcomas, but also genitourinary cancers and primary lung cancer; thus, pneumothorax in a patient with malignancy should prompt a look for metastatic disease. Chemotherapeutic agents, at times, can also induce SSP.
Interstitial lung diseases are associated with connective-tissue diseases. Ankylosing spondylitis may be noted when apical fibrosis is present; in fact, the typically low incidence of spontaneous pneumothorax in patients with ankylosing spondylitis (0.29%) increases 45-fold (to 13%) when apical fibrotic disease exists.
Lymphangioleiomyomatosis (LAM) may present with spontaneous pneumothorax. This disease is characterized by thin-walled cysts in women of childbearing age. Respiratory failure may lead to a need for lung transplantation, and previous pleurodesis is no longer an absolute contraindication for lung transplantation.
Thoracic endometriosis is a rare cause of recurrent pneumothorax (catamenial pneumothorax) in women that is thought to arise from endometriosis reaching the chest wall across the diaphragm (ie, its etiology may be primarily related to associated diaphragmatic defects). In a case series of 229 patients, catamenial pneumothorax caused by thoracic endometriosis was localized to the visceral pleura in 52% of patients and to the diaphragm in 39% of patients. Before recurrence, this condition may be initially diagnosed as primary spontaneous pneumothorax.
Iatrogenic and traumatic pneumothorax
Causes of iatrogenic pneumothorax include the following:
Transthoracic needle aspiration biopsy of pulmonary nodules (most common cause, accounting for 32-37% of cases)
Transbronchial or pleural biopsy
Central venous catheter insertion, usually subclavian or internal jugular 
Intercostal nerve block
Cardiopulmonary resuscitation (CPR) - Consider the possibility of a pneumothorax if ventilation becomes progressively more difficult.
Acute respiratory distress syndrome (ARDS) and positive pressure ventilation in the ICU - High peak airway pressures can translate into barotrauma in up to 3% of patients on a ventilator and up to 5% of patients with ARDS. 
Nasogastric feeding tube placement
Iatrogenic pneumothorax is a complication of medical or surgical procedures. It most commonly results from transthoracic needle aspiration. Other procedures commonly causing iatrogenic pneumothorax are therapeutic thoracentesis, pleural biopsy, central venous catheter insertion, transbronchial biopsy, positive pressure mechanical ventilation, and inadvertent intubation of the right mainstem bronchus. Therapeutic thoracentesis is complicated by pneumothorax 30% of the time when performed by inexperienced operators in contrast to only 4% of the time when performed by experienced clinicians.
The routine use of ultrasonography during diagnostic thoracentesis is associated with lower rates of pneumothorax (4.9% vs 10.3%) and need for tube thoracostomy (0.7% vs 4.1%). Similarly, in patients who are mechanically ventilated, thoracentesis guided by bedside ultrasonography without radiology support results in a relatively lower rate of pneumothorax.
Causes of traumatic pneumothorax include the following:
Trauma - Penetrating and nonpenetrating injury
High-risk occupation (eg, diving, flying)
Traumatic pneumothoraces can result from both penetrating and nonpenetrating lung injuries. Complications include hemopneumothorax and bronchopleural fistula. Traumatic pneumothoraces often can create a one-way valve in the pleural space (only letting in air without escape) and can lead to a tension pneumothorax.
The most common etiologies of tension pneumothorax are either iatrogenic or related to trauma, such as the following:
Blunt or penetrating trauma - Disruption of either the visceral or parietal pleura occurs and is often associated with rib fractures, though rib fractures are not necessary for tension pneumothorax to occur.
Barotrauma secondary to positive-pressure ventilation (PPV), especially when high amounts of positive end-expiratory pressure (PEEP) are used
Pneumoperitoneum [18, 19]
Fiberoptic bronchoscopy with closed lung biopsy 
Markedly displaced thoracic spine fractures
Acupuncture [21, 22, 23]
Preexisting Bochdalek hernia with trauma 
Colonoscopy  and gastroscopy have been implicated in case reports.
Percutaneous tracheostomy 
Conversion of idiopathic, spontaneous, simple pneumothorax to tension pneumothorax
Unsuccessful attempts to convert an open pneumothorax to a simple pneumothorax in which the occlusive dressing functions as a one-way valve
Tension pneumothorax occurs commonly in the ICU setting in patients who are ventilated with positive pressure, and practitioners must always consider this when changes in respiratory or hemodynamic status occur. Infants requiring ventilatory assistance and those with meconium aspiration have a particularly high risk for tension pneumothorax. Aspirated meconium may serve as a one-way valve and produce a tension pneumothorax.
Any penetrating wound that produces an abnormal passageway for gas exchange into the pleural spaces and that results in air trapping may produce a tension pneumothorax. Blunt trauma, with or without associated rib fractures, and incidents such as unrestrained head-on motor vehicle accidents, falls, and altercations involving laterally directed blows may also cause tension pneumothoraces.
Significant chest injuries carry an estimated 10-50% risk of associated pneumothorax; in about 50% of these cases, the pneumothorax may not be seen on standard radiographs and are therefore deemed occult. In one study, 12% of patients with asymptomatic chest stab wounds had a delayed pneumothorax or hemothorax. McPherson et al analyzed data from the Vietnam Wound Data and Munitions Effectiveness Team study and determined that tension pneumothorax was the cause of death in 3-4% of fatally wounded combat casualties.
Acupuncture is a traditional Chinese medicine technique used worldwide by alternative medical practitioners. Acupuncture's most frequently reported serious complication is pneumothorax; in one Japanese report of 55,291 acupuncture treatments, an approximate incidence of 1 pneumothorax in 5000 cases was documented.
The following factors may result in pneumomediastinum:
Acute generation of high intrathoracic pressures (often as a result of inhalational drug use, such smoking marijuana or inhalation of cocaine)
Respiratory tract infection
Trauma or surgical disruption of the oropharyngeal, esophageal, or respiratory mucosa
The epidemiologic data vary among the pneumothorax classifications.
Primary, secondary, and recurring spontaneous pneumothorax
It is likely that the incidence for spontaneous pneumothorax is underestimated. Up to 10% of patients may be asymptomatic, and others with mild symptoms may not present to a medical provider.
PSPs occur in people aged 20-30 years, with a peak incidence is in the early 20s. PSP is rarely observed in people older than 40 years. The age-adjusted incidence of PSP is 7.4-18 cases per 100,000 persons per year for men and 1.2-6 cases per 100,000 persons per year for women. The male-to-female ratio of age-adjusted rates is 6.2:1.
SSPs occur more frequently in patients aged 60-65 years. The age-adjusted incidence of SSP is 6.3 cases per 100,000 persons per year for men and 2.0 cases per 100,000 persons per year for women. The male-to-female ratio of age-adjusted rates is 3.2:1. Chronic obstructive pulmonary disease (COPD) is a common cause of secondary spontaneous pneumothorax that carries an incidence of 26 cases per 100,000 persons.
Smoking increases the risk of a first spontaneous pneumothorax by more than 20-fold in men and by nearly 10-fold in women compared with risks in nonsmokers. Increased risk of pneumothorax and recurrence appears to rise proportionally with number of cigarettes smoked.
In men, the risk of spontaneous pneumothorax is 102 times higher in heavy smokers than in nonsmokers. Spontaneous pneumothorax most frequently occurs in tall, thin men aged 20-40 years.
Iatrogenic and traumatic pneumothorax
Traumatic and tension pneumothoraces occur more frequently than spontaneous pneumothoraces, and the rate is undoubtedly increasing in US hospitals as intensive care treatment modalities have become increasingly dependent on positive-pressure ventilation, central venous catheter placement, and other causes that potentially induce iatrogenic pneumothorax.
Iatrogenic pneumothorax may cause substantial morbidity and, rarely, death. The incidence of iatrogenic pneumothorax is 5-7 per 10,000 hospital admissions, with thoracic surgery patients excluded because pneumothorax may be a typical outcome following these surgeries.
Pneumothorax occurs in 1-2% of all neonates, with a higher incidence in infants with neonatal respiratory distress syndrome. In one study, 19% of such patients developed a pneumothorax.
Tension pneumothorax is a complication in approximately 1-2% of the cases of idiopathic spontaneous pneumothorax. Until the late 1800s, tuberculosis was a primary cause of pneumothorax development. A 1962 study showed a frequency of pneumothorax of 1.4% in patients with tuberculosis.
The actual incidence of tension pneumothorax outside of a hospital setting is impossible to determine. Approximately 10-30% of patients transported to level-1 trauma centers in the United States receive prehospital decompressive needle thoracostomies; however, not all of these patients actually have a true tension pneumothorax. Although this occurrence rate may seem high, disregarding the diagnosis would probably result in unnecessary deaths. A review of military deaths from thoracic trauma suggests that up to 5% of combat casualties with thoracic trauma have tension pneumothorax at the time of death.
The overall incidence of tension pneumothorax in the intensive care unit (ICU) is unknown. The medical literature provides only glimpses of the frequency. In one report, of 2000 incidents reported to the Australian Incident Monitoring Study (AIMS), 17 involved actual or suspected pneumothoraces, and 4 of those were diagnosed as tension pneumothorax.
Catamenial pneumothorax is a rare phenomenon that generally occurs in women aged 30-50 years. It frequently begins 1-3 days after menses onset. The risk of thoracic endometriosis cannot be predicted from the site of peritoneal lesions.
Spontaneous pneumomediastinum generally occurs in young, healthy patients without serious underlying pulmonary disease, mostly in the second to fourth decades of life. A slight predominance of pneumomediastinum exists for males. This condition occurs in approximately 1 case per 10,000 hospital admissions.
The prognosis varies among the pneumothorax classifications.
Primary, secondary, and recurring spontaneous pneumothorax
Complete resolution of an uncomplicated pneumothorax takes approximately 10 days. PSP is typically benign and often resolves without medical attention. Many affected individuals do not seek medical attention for days after symptoms develop. This trend is important, because the incidence of reexpansion pulmonary edema increases in patients whose chest tubes have been placed 3 or more days after the pneumothorax occurred.
Recurrences usually strike within the first 6 months to 3 years. The 5-year recurrence rate is 28-32% for PSP and 43% for SSP.
Recurrences are more common among patients who smoke, patients with COPD and patients with AIDS. Predictors of recurrence include pulmonary fibrosis, younger age, and increased height-to-weight ratio. In a retrospective study of 182 consecutive patients with a newly diagnosed first episode of pneumothorax, a higher rate of recurrence was noted in taller patients, thin patients, and patients with SSP.
Patients who underwent bedside chest tube pleurodesis had cumulative rates of recurrence of 13% at 6 months, 16% at 1 year, and 27% at 3 years compared with 26%, 33%, and 50%, respectively. The agent used (tetracycline or gentamicin) did not have any significant impact on the recurrence rate.
Bullous lesions found on CT or at thoracoscopy and the presence of ELCs in PSP are also not predictive of recurrence. However, contralateral blebs were seen by CT scanning in higher frequency in the patients with contralateral recurrence (33 patients; 14%) than those without a contralateral recurrence in a retrospective study of 231 patients with PSP. Primary bilateral spontaneous pneumothorax (PBSP) was significantly more common in patients with lower body mass index (BMI) and among smokers. In this series, all patients with contralateral recurrence were treated surgically.
Although some authors view PSP as more of a nuisance than a major health threat, deaths have been reported. SSPs are more often life threatening, depending on the severity of the underlying disease and the size of the pneumothorax (1-17% mortality). In particular, compared with similar patients without pneumothorax, age-matched patients with COPD have a 3.5-fold increase in relative mortality when a spontaneous pneumothorax occurs, and their risk of recurrence rises with each occurrence. One study indicated that 5% of patients with COPD died before a chest tube was placed.
Patients with AIDS also have a high inpatient mortality rate of 25% and a median survival of 3 months after the pneumothorax. These data were derived from an era before highly active antiretroviral therapy (HAART) was available.
Tension pneumothorax arises from numerous causes and rapidly progresses to respiratory insufficiency, cardiovascular collapse, and, ultimately, death if not recognized and treated. Therefore, if the clinical picture fits a tension pneumothorax, it must be emergently treated before it results in hemodynamic instability and death.
Pneumomediastinum is generally a benign, self-limited condition. Malignant pneumomediastinum, or tension pneumomediastinum (unvented mediastinal or pulmonary adventitial air causing pressure so high that circulatory or ventilatory failure occurs), was first described in 1944; however, all patients described in this report had serious comorbid conditions, often related to trauma or in association with Boerhaave syndrome.
No reports of fatal outcomes in patients with spontaneous pneumomediastinum in the absence of underlying disease exist in the more recent literature. The mortality rate is as high as 70% in patients with pneumomediastinum secondary to Boerhaave syndrome, even with surgical intervention. Traumatic mediastinum, although present in up to 6% of patients does not portend serious injury.
Two important concerns that clinicians should educate patients with pneumothorax/resolving pneumothorax about are avoidance of air travel/travel to remote regions and prohibition of smoking. Patients should also be advised to wear safety belts and passive restraint devices while driving.
Avoid traveling by air or to remote areas
Patients should not travel by air or travel to remote sites until radiography shows complete resolution. Although commercial air travel achieves minimal change in gas volumes due to pressurization of the cabin, spontaneous pneumothorax has been described during commercial travel.
Patients with previous spontaneous pneumothoraces are at risk for recurrence and are advised not to dive unless thoracotomy or pleurodesis has been performed. Ascent from deep-sea diving causes gases to expand and can lead to pneumothorax in patients with bullae and blebs.
Smoking cessation is strongly advised for all patients. They should be assessed as to readiness to quit, to be educated about smoking cessation, and be provided with pharmacotherapy if ready to quit. Direct patients indicating a readiness to quit smoking to their primary care physician or offer referral for cessation management. This may include nicotine replacement and non-nicotine pharmacotherapy such as bupropion or varenicline.
Whether primary or secondary pneumothorax, smoking increases the likelihood of bleb rupture and recurrence, and it does so in a predictable, dose-related manner. Relative risk of bleb rupture and recurrence rises by up to a factor of 20.
For patient education information, see the Lung and Airway Center and Breathing Difficulties Center, as well as Collapsed Lung (Pneumothorax) and Chest Pain.
Tschopp JM, Rami-Porta R, Noppen M, Astoul P. Management of spontaneous pneumothorax: state of the art. Eur Respir J. 2006 Sep. 28(3):637-50. [Medline].
Sahn SA, Heffner JE. Spontaneous pneumothorax. N Engl J Med. 2000 Mar 23. 342(12):868-74. [Medline].
Noppen M, Dekeukeleire T, Hanon S, Stratakos G, Amjadi K, Madsen P. Fluorescein-enhanced autofluorescence thoracoscopy in patients with primary spontaneous pneumothorax and normal subjects. Am J Respir Crit Care Med. 2006 Jul 1. 174(1):26-30. [Medline].
Tabakoglu E, Ciftci S, Hatipoglu ON, Altiay G, Caglar T. Levels of superoxide dismutase and malondialdehyde in primary spontaneous pneumothorax. Mediators Inflamm. 2004 Jun. 13(3):209-10. [Medline].
Haraguchi S, Fukuda Y. Histogenesis of abnormal elastic fibers in blebs and bullae of patients with spontaneous pneumothorax: ultrastructural and immunohistochemical studies. Acta Pathol Jpn. 1993 Dec. 43(12):709-22. [Medline].
Gunji Y, Akiyoshi T, Sato T, Kurihara M, Tominaga S, Takahashi K. Mutations of the Birt Hogg Dube gene in patients with multiple lung cysts and recurrent pneumothorax. J Med Genet. 2007 Sep. 44(9):588-93. [Medline].
Lal A, Anderson G, Cowen M, Lindow S, Arnold AG. Pneumothorax and pregnancy. Chest. 2007 Sep. 132(3):1044-8. [Medline].
Chiu HT, Garcia CK. Familial spontaneous pneumothorax. Curr Opin Pulm Med. 2006 Jul. 12(4):268-72. [Medline].
Feldman AL, Sullivan JT, Passero MA, Lewis DC. Pneumothorax in polysubstance-abusing marijuana and tobacco smokers: three cases. J Subst Abuse. 1993. 5(2):183-6. [Medline].
Sihoe AD, Wong RH, Lee AT, et al. Severe acute respiratory syndrome complicated by spontaneous pneumothorax. Chest. 2004 Jun. 125(6):2345-51. [Medline].
Metersky ML, Colt HG, Olson LK, Shanks TG. AIDS-related spontaneous pneumothorax. Risk factors and treatment. Chest. 1995 Oct. 108(4):946-51. [Medline].
Flume PA, Strange C, Ye X, Ebeling M, Hulsey T, Clark LL. Pneumothorax in cystic fibrosis. Chest. 2005 Aug. 128(2):720-8. [Medline].
Leslie MD, Napier M, Glaser MG. Pneumothorax as a complication of tumour response to chemotherapy. Clin Oncol (R Coll Radiol). 1993. 5(3):181-2. [Medline].
Lee CC, Lee SH, Chang IJ, et al. Spontaneous pneumothorax associated with ankylosing spondylitis. Rheumatology (Oxford). 2005 Dec. 44(12):1538-41. [Medline].
Korom S, Canyurt H, Missbach A, et al. Catamenial pneumothorax revisited: clinical approach and systematic review of the literature. J Thorac Cardiovasc Surg. 2004 Oct. 128(4):502-8. [Medline].
Plewa MC, Ledrick D, Sferra JJ. Delayed tension pneumothorax complicating central venous catheterization and positive pressure ventilation. Am J Emerg Med. 1995 Sep. 13(5):532-5. [Medline].
de Lassence A, Timsit JF, Tafflet M, et al. Pneumothorax in the intensive care unit: incidence, risk factors, and outcome. Anesthesiology. 2006 Jan. 104(1):5-13. [Medline].
Miller JS, Itani KM, Oza MD, Wall MJ. Gastric rupture with tension pneumoperitoneum: a complication of difficult endotracheal intubation. Ann Emerg Med. 1997 Sep. 30(3):343-6. [Medline].
Hashmi S, Rogers SO. Tension pneumothorax with pneumopericardium. J Trauma. 2003 Jun. 54(6):1254. [Medline].
Iannoli ED, Litman RS. Tension pneumothorax during flexible fiberoptic bronchoscopy in a newborn. Anesth Analg. 2002 Mar. 94(3):512-3; table of contents. [Medline]. [Full Text].
Peuker E. Case report of tension pneumothorax related to acupuncture. Acupunct Med. 2004 Mar. 22(1):40-3. [Medline]. [Full Text].
Whale C, Hallam C. Tension pneumothorax related to acupuncture. Acupunct Med. 2004 Jun. 22(2):101; author reply 101-2. [Medline].
Zhao DY, Zhang GL. [Clinical analysis on 38 cases of pneumothorax induced by acupuncture or acupoint injection]. Zhongguo Zhen Jiu. 2009 Mar. 29(3):239-42. [Medline].
Dalton AM, Hodgson RS, Crossley C. Bochdalek hernia masquerading as a tension pneumothorax. Emerg Med J. 2004 May. 21(3):393-4. [Medline]. [Full Text].
Hearnshaw SA, Oppong K, Jaques B, Thompson NP. Tension pneumothorax as a complication of colonoscopy. Endoscopy. 2004 Feb. 36(2):190. [Medline]. [Full Text].
Brander L, Takala J. Tracheal tear and tension pneumothorax complicating bronchoscopy-guided percutaneous tracheostomy. Heart Lung. 2006 Mar-Apr. 35(2):144-5. [Medline].
McPherson JJ, Feigin DS, Bellamy RF. Prevalence of tension pneumothorax in fatally wounded combat casualties. J Trauma. 2006 Mar. 60(3):573-8. [Medline].
Yamashita H, Tsukayama H, Tanno Y, Nishijo K. Adverse events related to acupuncture. JAMA. 1998 Nov 11. 280(18):1563-4. [Medline].
Melton LJ 3rd, Hepper NG, Offord KP. Incidence of spontaneous pneumothorax in Olmsted County, Minnesota: 1950 to 1974. Am Rev Respir Dis. 1979 Dec. 120(6):1379-82. [Medline].
Gupta D, Hansell A, Nichols T, Duong T, Ayres JG, Strachan D. Epidemiology of pneumothorax in England. Thorax. 2000 Aug. 55(8):666-71. [Medline].
Bense L, Eklund G, Wiman LG. Smoking and the increased risk of contracting spontaneous pneumothorax. Chest. 1987 Dec. 92(6):1009-12. [Medline].
Huang TW, Lee SC, Cheng YL, Tzao C, Hsu HH, Chang H. Contralateral recurrence of primary spontaneous pneumothorax. Chest. 2007 Oct. 132(4):1146-50. [Medline].
Rezende-Neto JB, Hoffmann J, Al Mahroos M, et al. Occult pneumomediastinum in blunt chest trauma: clinical significance. Injury. 2010 Jan. 41(1):40-3. [Medline].
[Guideline] British Thoracic Society guidelines on respiratory aspects of fitness for diving. Thorax. 2003 Jan. 58(1):3-13. [Medline]. [Full Text].
Rodriguez RM, Hendey GW, Marek G, Dery RA, Bjoring A. A pilot study to derive clinical variables for selective chest radiography in blunt trauma patients. Ann Emerg Med. 2006 May. 47(5):415-8. [Medline].
Lopes JA, Frankel HL, Bokhari SJ, Bank M, Tandon M, Rabinovici R. The trauma bay chest radiograph in stable blunt-trauma patients: do we really need it?. Am Surg. 2006 Jan. 72(1):31-4. [Medline].
Shatz DV, de la Pedraja J, Erbella J, Hameed M, Vail SJ. Efficacy of follow-up evaluation in penetrating thoracic injuries: 3- vs. 6-hour radiographs of the chest. J Emerg Med. 2001 Apr. 20(3):281-4. [Medline].
Henry M, Arnold T, Harvey J,. BTS guidelines for the management of spontaneous pneumothorax. Thorax. 2003 May. 58 Suppl 2:ii39-52. [Medline].
Baumann MH, Strange C, Heffner JE, Light R, Kirby TJ, Klein J. Management of spontaneous pneumothorax: an American College of Chest Physicians Delphi consensus statement. Chest. 2001 Feb. 119(2):590-602. [Medline].
Light RW, Courtney Broaddus V. Pneumothorax, chylothorax, hemothorax, and fibrothorax. Textbook of Pulmonary Medicine. 3rd ed. 2000. 2043-66.
Ball CG, Kirkpatrick AW, Feliciano DV. The occult pneumothorax: what have we learned?. Can J Surg. 2009 Oct. 52(5):E173-9. [Medline]. [Full Text].
Barrios C, Tran T, Malinoski D, et al. Successful management of occult pneumothorax without tube thoracostomy despite positive pressure ventilation. Am Surg. 2008 Oct. 74(10):958-61. [Medline].
Busch M. Portable ultrasound in pre-hospital emergencies: a feasibility study. Acta Anaesthesiol Scand. 2006 Jul. 50(6):754-8. [Medline].
Zanobetti M, Poggioni C, Pini R. Can chest ultrasonography replace standard chest radiography for evaluation of acute dyspnea in the ED?. Chest. 2011 May. 139(5):1140-7. [Medline].
Dente CJ, Ustin J, Feliciano DV, Rozycki GS, Wyrzykowski AD, Nicholas JM, et al. The accuracy of thoracic ultrasound for detection of pneumothorax is not sustained over time: a preliminary study. J Trauma. 2007 Jun. 62(6):1384-9. [Medline].
Knudtson JL, Dort JM, Helmer SD, Smith RS. Surgeon-performed ultrasound for pneumothorax in the trauma suite. J Trauma. 2004 Mar. 56(3):527-30. [Medline].
Dulchavsky SA, Schwarz KL, Kirkpatrick AW, Billica RD, Williams DR, Diebel LN, et al. Prospective evaluation of thoracic ultrasound in the detection of pneumothorax. J Trauma. 2001 Feb. 50(2):201-5. [Medline].
Brook OR, Beck-Razi N, Abadi S, Filatov J, Ilivitzki A, Litmanovich D, et al. Sonographic detection of pneumothorax by radiology residents as part of extended focused assessment with sonography for trauma. J Ultrasound Med. 2009 Jun. 28(6):749-55. [Medline].
Hernandez C, Shuler K, Hannan H, Sonyika C, Likourezos A, Marshall J. C.A.U.S.E.: Cardiac arrest ultra-sound exam--a better approach to managing patients in primary non-arrhythmogenic cardiac arrest. Resuscitation. 2008 Feb. 76(2):198-206. [Medline].
Sartori S, Tombesi P, Trevisani L, Nielsen I, Tassinari D, Abbasciano V. Accuracy of transthoracic sonography in detection of pneumothorax after sonographically guided lung biopsy: prospective comparison with chest radiography. AJR Am J Roentgenol. 2007 Jan. 188(1):37-41. [Medline].
Zhang M, Liu ZH, Yang JX, Gan JX, Xu SW, You XD, et al. Rapid detection of pneumothorax by ultrasonography in patients with multiple trauma. Crit Care. 2006. 10(4):R112. [Medline]. [Full Text].
Shostak E, Brylka D, Krepp J, Pua B, Sanders A. Bedside sonography for detection of postprocedure pneumothorax. J Ultrasound Med. 2013 Jun. 32(6):1003-9. [Medline].
Slater A, Goodwin M, Anderson KE, Gleeson FV. COPD can mimic the appearance of pneumothorax on thoracic ultrasound. Chest. 2006 Mar. 129(3):545-50. [Medline].
Lichtenstein D, Meziere G, Biderman P, Gepner A. The "lung point": an ultrasound sign specific to pneumothorax. Intensive Care Med. 2000 Oct. 26(10):1434-40. [Medline].
Miller AC, Harvey JE. Guidelines for the management of spontaneous pneumothorax. Standards of Care Committee, British Thoracic Society [published erratum appears in BMJ 1993 Jul 31;307(6899):308]. BMJ. 1993 Jul 10. 307(6896):114-6. [Medline].
Contou D, Razazi K, Katsahian S, Maitre B, Mekontso-Dessap A, Brun-Buisson C, et al. Small-bore catheter versus chest tube drainage for pneumothorax. Am J Emerg Med. 2012 Jan 2. [Medline].
Bense L, Lewander R, Eklund G, et al. Nonsmoking, non-alpha 1-antitrypsin deficiency-induced emphysema in nonsmokers with healed spontaneous pneumothorax, identified by computed tomography of the lungs. Chest. 1993 Feb. 103(2):433-8. [Medline].
Moore FO, Goslar PW, Coimbra R, et al. Blunt Traumatic Occult Pneumothorax: Is Observation Safe?-Results of a Prospective, AAST Multicenter Study. J Trauma. 2011 May. 70(5):1019-1025. [Medline].
Delius RE, Obeid FN, Horst HM, Sorensen VJ, Fath JJ, Bivins BA. Catheter aspiration for simple pneumothorax. Experience with 114 patients. Arch Surg. 1989 Jul. 124(7):833-6. [Medline].
Noppen M, Baumann MH. Pathogenesis and treatment of primary spontaneous pneumothorax: an overview. Respiration. 2003 Jul-Aug. 70(4):431-8. [Medline].
Zehtabchi S, Rios CL. Management of emergency department patients with primary spontaneous pneumothorax: needle aspiration or tube thoracostomy?. Ann Emerg Med. 2008 Jan. 51(1):91-100, 100.e1. [Medline].
Marquette CH, Marx A, Leroy S, Vaniet F, Ramon P, Caussade S. Simplified stepwise management of primary spontaneous pneumothorax: a pilot study. Eur Respir J. 2006 Mar. 27(3):470-6. [Medline].
Ferrie EP, Collum N, McGovern S. The right place in the right space? Awareness of site for needle thoracocentesis. Emerg Med J. 2005 Nov. 22(11):788-9. [Medline]. [Full Text].
Wax DB, Leibowitz AB. Radiologic assessment of potential sites for needle decompression of a tension pneumothorax. Anesth Analg. 2007 Nov. 105(5):1385-8, table of contents. [Medline]. [Full Text].
Harcke HT, Pearse LA, Levy AD, Getz JM, Robinson SR. Chest wall thickness in military personnel: implications for needle thoracentesis in tension pneumothorax. Mil Med. 2007 Dec. 172(12):1260-3. [Medline].
Sanchez LD, Straszewski S, Saghir A, et al. Anterior versus lateral needle decompression of tension pneumothorax: comparison by computed tomography chest wall measurement. Acad Emerg Med. 2011 Oct. 18(10):1022-6. [Medline].
Givens ML, Ayotte K, Manifold C. Needle thoracostomy: implications of computed tomography chest wall thickness. Acad Emerg Med. 2004 Feb. 11(2):211-3. [Medline].
Zengerink I, Brink PR, Laupland KB, Raber EL, Zygun D, Kortbeek JB. Needle thoracostomy in the treatment of a tension pneumothorax in trauma patients: what size needle?. J Trauma. 2008 Jan. 64(1):111-4. [Medline].
Almoosa KF, Ryu JH, Mendez J, Huggins JT, Young LR, Sullivan EJ. Management of pneumothorax in lymphangioleiomyomatosis: effects on recurrence and lung transplantation complications. Chest. 2006 May. 129(5):1274-81. [Medline].
Sedrakyan A, van der Meulen J, Lewsey J, Treasure T. Video assisted thoracic surgery for treatment of pneumothorax and lung resections: systematic review of randomised clinical trials. BMJ. 2004 Oct 30. 329(7473):1008. [Medline].
Schramel FM, Postmus PE, Vanderschueren RG. Current aspects of spontaneous pneumothorax. Eur Respir J. 1997 Jun. 10(6):1372-9. [Medline].
Chen JS, Hsu HH, Huang PM, Kuo SW, Lin MW, Chang CC, et al. Thoracoscopic Pleurodesis for Primary Spontaneous Pneumothorax With High Recurrence Risk: A Prospective Randomized Trial. Ann Surg. 2012 Feb 8. [Medline].
Gonfiotti A, Santini PF, Jaus M, et al. Safety and effectiveness of a new fibrin pleural air leak sealant: a multicenter, controlled, prospective, parallel-group, randomized clinical trial. Ann Thorac Surg. 2011 Oct. 92(4):1217-25. [Medline].
O'Rourke JP, Yee ES. Civilian spontaneous pneumothorax. Treatment options and long-term results. Chest. 1989 Dec. 96(6):1302-6. [Medline].
Devanand A, Koh MS, Ong TH, et al. Simple aspiration versus chest-tube insertion in the management of primary spontaneous pneumothorax: a systematic review. Respir Med. 2004 Jul. 98(7):579-90. [Medline].
Loddenkemper R, Schonfeld N. Medical thoracoscopy. Curr Opin Pulm Med. 1998 Jul. 4(4):235-8. [Medline].
Almind M, Lange P, Viskum K. Spontaneous pneumothorax: comparison of simple drainage, talc pleurodesis, and tetracycline pleurodesis. Thorax. 1989 Aug. 44(8):627-30. [Medline].
Baumann MH, Strange C. Treatment of spontaneous pneumothorax: a more aggressive approach?. Chest. 1997 Sep. 112(3):789-804. [Medline].
van den Brande P, Staelens I. Chemical pleurodesis in primary spontaneous pneumothorax. Thorac Cardiovasc Surg. 1989 Jun. 37(3):180-2. [Medline].