Overview Show
Practice EssentialsPneumothorax 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 symptomsThe presentation of patients with pneumothorax varies depending on the following types of pneumothorax and ranges from completely asymptomatic to life-threatening respiratory distress:
See Clinical Presentation for more detail. DiagnosisHistory 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:
Cardiovascular findings may include the following:
Common findings among the types of pneumothoraces include the following:
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:
See Workup for more detail. ManagementAlthough 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. [1] The range of medical therapeutic options for pneumothorax includes the following:
Surgery 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:
Pharmacotherapy The following medications may be used to aid in the management of patients with pneumothorax:
See Treatment and Medication for more detail. BackgroundPneumothorax 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 pneumothoraxSpontaneous 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). [2] 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. [2] 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 pneumothoraxIatrogenic 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. Tension pneumothoraxA 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. PneumomediastinumPneumomediastinum 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. AnatomyThe 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. PathophysiologySpontaneous pneumothoraxSpontaneous 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. [3] 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. [4] 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. [5] In one study, erythrocyte superoxide dismutase activity was significantly lower and plasma malondialdehyde levels higher in patients with PSP than in normal control subjects. [4] 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. [6] A germ-line mutation to this gene has been found in five patients, and genetic testing is now available. Tension pneumothoraxTension 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. PneumomediastinumWith 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 pneumothoraxRisks factors for primary spontaneous pneumothorax (PSP) include the following:
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. [2] Nonsmokers with PSP had CT scan ELC abnormalities of 80% compared with a rate of 0% among nonsmoker controls without PSP. [2] 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. [7] The cases were all managed successfully with simple aspiration or video-assisted thoracoscopic surgery (VATS), and no harm occurred to mother or fetus. [7] 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. [8] 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:
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. [11] 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). [12] 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. [13] 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. [14] 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. [15] Before recurrence, this condition may be initially diagnosed as primary spontaneous pneumothorax. Iatrogenic and traumatic pneumothoraxCauses of iatrogenic pneumothorax include the following:
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:
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. Tension pneumothoraxThe most common etiologies of tension pneumothorax are either iatrogenic or related to trauma, such as the following:
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. [27] 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. [28] PneumomediastinumThe following factors may result in pneumomediastinum:
EpidemiologyPrimary, secondary, and recurring spontaneous pneumothoraxIt 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. [29] 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. [30] 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. [31] 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 pneumothoraxTraumatic 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 pneumothoraxTension 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. [27] 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 pneumothoraxCatamenial 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. [15] PneumomediastinumSpontaneous 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. PrognosisPrimary, secondary, and recurring spontaneous pneumothoraxComplete 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. [32] 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 pneumothoraxTension 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. PneumomediastinumPneumomediastinum 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. [33] Patient EducationTwo 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. Avoidance of travel by air or to remote areasPatients 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. [34] Ascent from deep-sea diving causes gases to expand and can lead to pneumothorax in patients with bullae and blebs. Smoking cessationSmoking 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.
Author Brian J Daley, MD, MBA, FACS, FCCP, CNSC Professor and Program Director, Department of Surgery, Chief, Division of Trauma and Critical Care, University of Tennessee Health Science Center College of Medicine Brian J Daley, MD, MBA, FACS, FCCP, CNSC is a member of the following medical societies: American Association for the Surgery of Trauma, Eastern Association for the Surgery of Trauma, Southern Surgical Association, American College of Chest Physicians, American College of Surgeons, American Medical Association, Association for Academic Surgery, Association for Surgical Education, Shock Society, Society of Critical Care Medicine, Southeastern Surgical Congress, Tennessee Medical Association Disclosure: Nothing to disclose. Coauthor(s) Rebecca Bascom, MD, MPH Professor of Medicine, Department of Medicine, Division of Pulmonary, Allergy, and Critical Care Medicine, Pennsylvania State College of Medicine, Milton S Hershey Medical Center; Graduate Faculty Member, Pennsylvania State University College of Medicine and The Huck Institutes of the Life Sciences Rebecca Bascom, MD, MPH is a member of the following medical societies: American Thoracic Society Disclosure: Nothing to disclose. Shoaib Alam, MD Staff Clinician, Pulmonary and Vascular Medicine, National Heart, Lung, and Blood Institute, National Institutes of Health Shoaib Alam, MD is a member of the following medical societies: American College of Chest Physicians, American Thoracic Society, Society of Critical Care Medicine, International Society for Magnetic Resonance in Medicine, European Respiratory Society, Pennsylvania Thoracic Society Disclosure: Nothing to disclose. Chief Editor Mary C Mancini, MD, PhD, MMM Mary C Mancini, MD, PhD, MMM is a member of the following medical societies: American Association for Thoracic Surgery, American College of Surgeons, American Surgical Association, Phi Beta Kappa, Society of Thoracic Surgeons Disclosure: Nothing to disclose. Acknowledgements Erik D Barton, MD, MS Associate Director, Assistant Professor, Department of Surgery, Division of Emergency Medicine, University of Utah Health Sciences Center Erik D Barton, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American College of Sports Medicine, American Medical Association, and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. Marc D Basson, MD, PhD, MBA, FACS Professor, Chair, Department of Surgery, Assistant Dean for Faculty Development in Research, Michigan State University College of Human Medicine Marc D Basson, MD, PhD, MBA, FACS is a member of the following medical societies: Alpha Omega Alpha, American College of Surgeons, American Gastroenterological Association, Phi Beta Kappa, and Sigma Xi Disclosure: Nothing to disclose. H Scott Bjerke, MD, FACS Clinical Associate Professor, Department of Surgery, University of Missouri-Kansas City School of Medicine; Medical Director of Trauma Services, Research Medical Center; Clinical Professor, Department of Surgery, Kansas City University of Medicine and Biosciences H Scott Bjerke, MD, FACS is a member of the following medical societies: American Association for the History of Medicine, American Association for the Surgery of Trauma, American College of Surgeons, Association for Academic Surgery, Eastern Association for the Surgery of Trauma, Midwest Surgical Association, National Association of EMS Physicians, Pan-Pacific Surgical Association, Royal Society of Medicine, Southwestern Surgical Congress, andWilderness Medical Society Disclosure: Nothing to disclose. Paul Blackburn, DO, FACOEP, FACEP Attending Physician, Department of Emergency Medicine, Maricopa Medical Center Paul Blackburn, DO, FACOEP, FACEP is a member of the following medical societies: American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, American Medical Association, and Arizona Medical Association Disclosure: Nothing to disclose. Jeffrey Glenn Bowman, MD, MS Consulting Staff, Highfield MRI Disclosure: Nothing to disclose. Andrew K Chang, MD Associate Professor, Department of Emergency Medicine, Albert Einstein College of Medicine, Montefiore Medical Center Andrew K Chang, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. John Geibel, MD, DSc, MA Vice Chair and Professor, Department of Surgery, Section of Gastrointestinal Medicine, and Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director, Surgical Research, Department of Surgery, Yale-New Haven Hospital John Geibel, MD, DSc, MA is a member of the following medical societies: American Gastroenterological Association, American Physiological Society, American Society of Nephrology, Association for Academic Surgery, International Society of Nephrology, New York Academy of Sciences, and Society for Surgery of the Alimentary Tract Disclosure: AMGEN Royalty Consulting; ARdelyx Ownership interest Board membership Tunc Iyriboz, MD Chief, Division of Clinical Image Management, Assistant Professor, Department of Radiology, Hershey Medical Center, Pennsylvania State University Tunc Iyriboz, MD is a member of the following medical societies: American College of Radiology, American Medical Association, and Radiological Society of North America Disclosure: Nothing to disclose. Seema Jain Pennsylvania State University College of Medicine Disclosure: Nothing to disclose. Rick Kulkarni, MD Attending Physician, Department of Emergency Medicine, Cambridge Health Alliance, Division of Emergency Medicine, Harvard Medical School Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine Disclosure: WebMD Salary Employment Eric L Legome, MD Chief, Department of Emergency Medicine, Kings County Hospital Center; Associate Professor, Department of Emergency Medicine, New York Medical College Eric L Legome, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, Council of Emergency Medicine Residency Directors, and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. Pinaki Mukherji, MD Assistant Professor, Attending Physician, Department of Emergency Medicine, Montefiore Medical Center Pinaki Mukherji, MD is a member of the following medical societies: American College of Emergency Physicians Disclosure: Nothing to disclose. Robert E O'Connor, MD, MPH Professor and Chair, Department of Emergency Medicine, University of Virginia Health System Robert E O'Connor, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physician Executives, American Heart Association, American Medical Association, Medical Society of Delaware, National Association of EMS Physicians, Society for Academic Emergency Medicine, and Wilderness Medical Society Disclosure: Nothing to disclose. Benson B Roe, MD Emeritus Chief, Division of Cardiothoracic Surgery, Emeritus Professor, Department of Surgery, University of California at San Francisco Medical Center Benson B Roe, MD is a member of the following medical societies: Alpha Omega Alpha, American Association for Thoracic Surgery, American College of Cardiology, American College of Surgeons, American Heart Association, American Medical Association, American Society for Artificial Internal Organs, American Surgical Association, California Medical Association, Society for Vascular Surgery, Society of Thoracic Surgeons, and Society of University Surgeons Disclosure: Nothing to disclose. Joseph A Salomone III, MD Associate Professor and Attending Staff, Truman Medical Centers, University of Missouri-Kansas City School of Medicine; EMS Medical Director, Kansas City, Missouri Joseph A Salomone III, MD is a member of the following medical societies: American Academy of Emergency Medicine, National Association of EMS Physicians, and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. Daniel S Schwartz, MD, FACS Assistant Clinical Professor of Cardiothoracic Surgery, Mount Sinai School of Medicine; Chief of Thoracic Surgery, Huntington Hospital Daniel S Schwartz, MD, FACS is a member of the following medical societies: American College of Chest Physicians, American College of Surgeons, Society of Thoracic Surgeons, and Western Thoracic Surgical Association Disclosure: Nothing to disclose. Robert L Sheridan, MD Assistant Chief of Staff, Chief of Burn Surgery, Shriners Burns Hospital; Associate Professor of Surgery, Department of Surgery, Division of Trauma and Burns, Massachusetts General Hospital and Harvard Medical School Robert L Sheridan, MD is a member of the following medical societies: American Academy of Pediatrics, American Association for the Surgery of Trauma, American Burn Association, and American College of Surgeons Disclosure: Nothing to disclose. Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Medscape Salary Employment Milos Tucakovic, MD Fellow, Department of Internal Medicine, Sections of Pulmonary Disease, Allergy and Critical Care Medicine, Milton S Hershey Medical Center, Pennsylvania State College of Medicine Milos Tucakovic, MD is a member of the following medical societies: American College of Physicians and American Medical Association Disclosure: Nothing to disclose. Which interventions would the nurse perform at the end of a physical examination in a hospital setting select all that apply?Which interventions should the nurse perform at the end of a physical examination in a hospital setting? Return the bedside table to its normal position. Ensure that the patient can access the call button in the room. Keep the television or any equipment the way it was originally.
Which measures eliminate confusion artifacts while evaluating the body sounds during auscultation?Eliciting a deep tendon reflex is a part of the percussion technique. Which measures will help the nurse eliminate any confusing artifacts while evaluating the body sounds during auscultation? Friction between the chest hairs and the stethoscope endpiece may interfere with the body sounds.
Which type of sounds is Auscultated with the bell of the stethoscope quizlet?What type of body sounds will the nurse be able to hear with the bell of the stethoscope? The bell is a concave cup that best transmits low-pitched sounds. The nurse should hold the bell of the stethoscope very lightly on the skin to listen to low-pitched sounds such as heart murmurs.
Which assessment technique would the nurse use to determine the patients temperature?Auscultation: The nurse assesses the carotids for the presence of any abnormal bruits. Palpation: The peripheral veins are gently touched to determine the temperature of the skin, the presence of any tenderness and swelling.
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Which intervention improve the accuracy of Auscultating the lungs of a patient with excessive chest hair?
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