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Pneumothorax

A pneumothorax is a medical condition characterized by the accumulation of air in the pleural space—the potential cavity between the visceral and parietal pleurae surrounding the lungs—leading to partial or of the affected due to increased pressure disrupting the normal negative . This air entry typically results from a rupture in the or pleural membrane, and the condition can range from asymptomatic small collections to life-threatening emergencies, particularly in cases of tension pneumothorax where air enters but cannot escape, causing mediastinal shift and cardiovascular compromise. Pneumothoraces are classified into several types based on and presentation. Primary spontaneous pneumothorax occurs without apparent underlying , often due to the rupture of subpleural blebs or bullae, and is more common in young, tall, thin males aged 20–40 who smoke. Secondary spontaneous pneumothorax arises in the context of pre-existing pulmonary conditions such as (COPD), , , or , with higher incidence in older adults around ages 60–65. Traumatic pneumothorax results from blunt or penetrating chest injuries, such as fractures or stab wounds, while iatrogenic cases stem from medical interventions like placement or . pneumothorax, a severe subtype, is a often associated with or from positive-pressure ventilation, leading to rapid hemodynamic instability. The primary causes of pneumothorax involve disruptions allowing air to enter the pleural space, including spontaneous rupture of apical blebs in otherwise healthy lungs or bullae in diseased lungs, direct trauma to the chest wall or lung parenchyma, and procedural complications. Risk factors encompass male sex, smoking (which increases risk up to 20-fold), family history or genetic predispositions like Marfan syndrome, tall and slender body habitus, previous pneumothorax episodes, and underlying lung diseases such as emphysema or tuberculosis. Additional risks include scuba diving, cocaine use, and pregnancy in rare cases. Clinically, pneumothorax presents with sudden-onset sharp on the affected side, often worsened by breathing, accompanied by dyspnea or whose severity correlates with the extent of lung collapse. In tension pneumothorax, symptoms escalate to include , , , jugular venous distension, and , signaling . Small, pneumothoraces may be incidental findings, while larger ones can cause rapid respiratory distress. Diagnosis relies on clinical evaluation, including history and physical exam findings like decreased breath sounds and hyperresonance on percussion, confirmed by imaging: upright chest X-ray is the gold standard, showing a visible pleural line and absent markings; scans provide detailed assessment for small or occult pneumothoraces; and offers rapid bedside detection with high sensitivity. In unstable patients, immediate needle decompression may precede imaging. Management varies by size, symptoms, and type: small, stable primary pneumothoraces may resolve with and supplemental oxygen to accelerate air reabsorption, while symptomatic or larger ones require needle aspiration or thoracostomy to evacuate air and re-expand the . Tension pneumothorax demands urgent needle followed by definitive tube placement. Recurrent or persistent cases may necessitate surgical interventions like (VATS) for bleb resection or to prevent reaccumulation. Complications include recurrent pneumothorax (up to 50% without intervention), persistent air leaks, , or in secondary cases.

Signs and symptoms

General presentation

Pneumothorax commonly manifests with a sudden onset of sharp, unilateral and progressive , which are the primary symptoms reported by patients. The is typically pleuritic in nature, worsening with , and may radiate to the ipsilateral , reflecting irritation of the pleural surfaces. Physical examination reveals characteristic findings on the affected side, including decreased or absent breath sounds upon and hyperresonance to percussion due to the presence of air in the pleural space. Asymmetrical chest expansion and decreased tactile may also be noted, though these signs can be subtle in smaller pneumothoraces. Tracheal deviation toward the unaffected side occurs infrequently and only mildly if at all in non-tension cases, distinguishing it from more pronounced shifts in severe variants. Additional associated symptoms in moderate pneumothorax include a non-productive , generalized , , and signs of such as or , which reflect the impaired and increased respiratory effort. The severity of these manifestations correlates with the extent of lung collapse; small pneumothoraces, often involving less than 15-20% of the hemithorax, may remain and go unnoticed, whereas larger ones lead to marked respiratory distress and hemodynamic changes. In contrast, tension pneumothorax represents a rapidly deteriorating form with profound instability.

Tension pneumothorax

Tension pneumothorax represents a critical, life-threatening subtype of pneumothorax in which air accumulates progressively in the pleural space under increasing , leading to cardiopulmonary collapse if untreated. This condition arises when a pleural defect functions as a one-way valve, permitting air entry into the during inspiration while preventing its escape during expiration, thereby elevating intrathoracic and causing ipsilateral collapse. The escalating shifts the mediastinum toward the contralateral side, compressing the great vessels and heart, which impairs venous return to the right atrium and reduces , ultimately resulting in . The clinical signs of pneumothorax include severe respiratory distress with and use of muscles, profound refractory to fluid , jugular venous distension due to elevated , and marked away from the affected side. As the condition advances, patients often develop from and altered mental status secondary to cerebral hypoperfusion. These manifestations distinguish pneumothorax from the milder, stable symptoms that may occur in general pneumothorax presentation and can progress to this state if unchecked. Tension pneumothorax typically has a rapid onset, often triggered by penetrating or that creates the valvular defect, or by spontaneous rupture of subpleural blebs in otherwise healthy individuals or those with underlying disease. It was first widely recognized as a during among battlefield casualties with thoracic injuries, where high mortality rates—around 25% for such wounds—highlighted the need for urgent to prevent fatal outcomes.

Causes

Primary spontaneous pneumothorax

Primary spontaneous pneumothorax () is defined as the accumulation of air in the pleural space causing partial or complete lung collapse in individuals without apparent underlying lung disease or , typically presenting as a first episode in otherwise healthy young adults. It predominantly affects tall, thin males aged 15 to 35 years, though it can occur in females as well. Genetic factors, including disorders such as and Ehlers-Danlos syndrome, can predispose individuals to PSP through weakened pleural structures. Family history also increases risk. The incidence of PSP is estimated at 7.4 to 18 cases per 100,000 population annually in males and 1.2 to 6 cases per 100,000 in females, with higher rates observed in populations with greater prevalence. is a major modifiable risk factor, increasing the relative risk of a first PSP episode by approximately 22-fold in males and 9-fold in females compared to nonsmokers. Other predisposing factors include a tall, thin habitus, which may contribute to increased gradients at the apices. Pathogenesis involves the rupture of subpleural blebs or bullae—small, air-filled sacs on the visceral pleura—leading to air leakage into the pleural space; these lesions are identified in up to 77% of cases via or . Congenital weaknesses in the visceral pleura, such as areas of pleural porosity or disrupted mesothelial cells, are often implicated, with ruptures frequently occurring at the apices due to higher . Precipitating events like Valsalva maneuvers (e.g., forceful coughing or straining) can exacerbate these weaknesses by transiently increasing intra-alveolar pressure. In contrast, secondary spontaneous pneumothorax arises in the context of pre-existing pulmonary disease. Without intervention, the recurrence rate for PSP is high, ranging from 21% to 54% within 1 to 2 years of the initial , with an overall risk of approximately 32%. Factors such as persistent blebs or continued may elevate this risk further.

Secondary spontaneous pneumothorax

Secondary spontaneous pneumothorax (SSP) refers to the accumulation of air in the pleural space causing collapse in individuals with preexisting , distinguishing it from primary spontaneous pneumothorax that occurs in otherwise healthy lungs. This condition arises when structural weaknesses in diseased tissue lead to air leakage into the , often resulting in more severe symptoms and complications due to reduced respiratory reserve. SSP typically presents with acute dyspnea, , and , exacerbated by the underlying that impairs compliance and . The most common underlying cause of SSP is (COPD), particularly , accounting for 50-70% of cases through the formation and rupture of subpleural bullae. Other frequent etiologies include , where bronchiectasis and air trapping predispose to alveolar rupture; interstitial lung diseases such as , characterized by subpleural honeycombing; and infections like , which can erode lung parenchyma leading to cavities that breach the pleura. These conditions weaken the lung's visceral pleura and alveolar walls, facilitating air escape under normal ventilatory pressures. SSP predominantly affects older patients, with a peak incidence between 60 and 65 years and a notable rise after age 50, reflecting the cumulative burden of diseases. Recurrence rates are substantially higher than in primary spontaneous pneumothorax, reaching 40-80% without , due to persistent diseased tissue vulnerable to repeated rupture. Mortality associated with SSP ranges from 1-16%, attributed to compromised pulmonary function, comorbidities, and challenges in achieving lung re-expansion. Pathophysiologically, SSP results from the rupture of diseased alveoli or the development of bronchopleural fistulas, where air tracks from damaged airways into the pleural space, often amplified by coughing or positive pressure ventilation in compromised lungs. In contrast to primary spontaneous pneumothorax, which involves idiopathic bleb rupture in healthy individuals with lower overall risk, SSP's disease-driven mechanism heightens morbidity through ongoing and . A notable example is in patients with AIDS, where significantly elevates pneumothorax risk, with reported incidences of 5-10%—substantially higher than in the general —due to subpleural and formation.

Traumatic pneumothorax

Traumatic pneumothorax occurs when air enters the pleural space due to direct injury to the chest wall or lung parenchyma from blunt or penetrating trauma, resulting in partial or complete lung collapse. This condition is a common sequela of thoracic injuries and can arise from various mechanisms that breach the integrity of the visceral or parietal pleura. Unlike spontaneous forms, traumatic pneumothorax is invariably linked to external physical forces, such as those encountered in accidents or assaults. The primary types include closed, open, and hemopneumothorax. Closed pneumothorax typically results from blunt force , such as fractures or sudden deceleration, which increases intrathoracic pressure and causes alveolar rupture, allowing air to leak into the without an external . Open pneumothorax, often termed a "sucking chest ," involves a penetrating that creates a defect in the chest wall larger than the tracheal opening, permitting bidirectional air flow between the atmosphere and pleural space during respiration. Hemopneumothorax combines pneumothorax with , occurring when the also lacerates blood vessels, leading to both air and blood accumulation in the pleural space; this is particularly prevalent in penetrating traumas affecting the periphery. Common scenarios precipitating traumatic pneumothorax include collisions, which account for approximately 40-70% of cases in cohorts, followed by falls from height and penetrating injuries like stab or wounds. Incidence varies by population and injury severity, affecting 20-30% of patients with chest and up to 28% in broader series. Associated injuries frequently include concurrent rib fractures, which occur in over half of cases and elevate mortality risk; pulmonary contusions, leading to impaired ; and diaphragmatic injuries, which may complicate and require surgical intervention. pneumothorax can develop rapidly in these settings due to a one-way , exacerbating hemodynamic instability.

Iatrogenic pneumothorax

Iatrogenic pneumothorax refers to the accumulation of air in the pleural space resulting from medical procedures or interventions, distinguishing it from spontaneous or traumatic forms by its procedural . Recognition typically occurs through post-procedure symptoms such as sudden dyspnea, oxygen desaturation, pleuritic , , or , often prompting immediate chest imaging for confirmation. The primary causes of iatrogenic pneumothorax include insertion, leading to , and procedures such as or . Central line placement, especially via the subclavian approach, carries a of 1-6.6%, with subclavian sites posing 0.45-3.1% incidence compared to less than 0.2% for internal jugular access, and up to 30% of all mechanical complications from catheter insertion involving pneumothorax. contributes through , with an overall incidence of 3-6% in ventilated patients and up to 5% specifically in (ICU) settings; this escalates in high-pressure scenarios. has a pneumothorax of 2-30%, while transthoracic needle biopsies range from 5-25%, often requiring chest tube intervention in 3.9-15% of cases depending on patient factors like underlying lung disease. Particularly high-risk procedures involve positive pressure ventilation in patients with (ARDS), where incidence can reach 18.9-20%, driven by elevated airway pressures and underlying lung fragility. In contrast to traumatic pneumothorax from external injury, iatrogenic cases arise solely from procedural mishaps, such as needle puncture of the pleura or alveolar rupture from overdistension. Emphasis on prevention is crucial in clinical practice, with guidance reducing risks by up to 70%, standardized protocols for minimizing pneumothorax to under 5%, and strategies like low tidal volumes (6 mL/kg) lowering in ARDS to below 10%. Simulation training and experienced operators further mitigate incidence across these interventions.

Neonatal pneumothorax

Neonatal pneumothorax refers to the accumulation of air in the pleural space of newborns, often linked to the unique vulnerabilities of lungs that may reference general pathophysiological mechanisms of lung collapse but with adaptations such as reduced and compliant chest walls exacerbating air leaks. The incidence is approximately 1-2% among all newborns, though it is substantially higher in preterm infants requiring assisted , ranging from 5-10% in those with neonatal lung disease to up to 30% in mechanically ventilated cases. Common etiologies include assisted ventilation, which increases intrathoracic pressure leading to alveolar rupture, particularly in preterm infants where it accounts for a significant proportion of cases. , occurring when the newborn inhales meconium-stained , causes airway obstruction and inflammation that predispose to pneumothorax, especially in term or post-term infants. , due to deficiency in preterm neonates, further heightens risk through uneven ventilation and barotrauma during supportive therapies. Symptoms in affected neonates may include grunting respirations, , and rapid breathing, reflecting impaired and respiratory effort; however, many cases in term infants are asymptomatic, discovered incidentally on . Physical signs can involve decreased breath sounds on the affected side and nasal flaring, though severe presentations like are less typical and more associated with underlying conditions such as . A 2021 study by Andersson et al. in the post-surfactant era analyzed 75 cases from 2011-2017, reporting an incidence of 3.1 per 1000 live births and noting milder symptoms overall, with (77%), (56%), and grunting (47%) as predominant features, alongside low rates of invasive intervention (16%) and mortality (3%). Onset occurred in all cases within 48 hours of birth, underscoring the acute perinatal nature in this era of improved therapies.

Pathophysiology

Mechanism of lung collapse

The pleural cavity is a thin, potential space between the visceral pleura, which directly covers the lung surface, and the parietal pleura, which lines the inner aspect of the thoracic cage, diaphragm, and mediastinum. This space normally contains a small volume of pleural fluid that reduces friction during respiratory movements and maintains a subatmospheric pressure, typically around -5 cm H₂O at functional residual capacity (FRC), generated by the balanced opposing forces of lung elastic recoil pulling inward and chest wall expansion pulling outward. This negative intrapleural pressure is essential for keeping the lungs expanded and apposed to the chest wall during the respiratory cycle. Pneumothorax develops when air enters the , breaching the integrity of either the visceral or parietal pleura and thereby disrupting the gradient. Common routes of air entry include rupture of alveoli or subpleural blebs through the visceral pleura, direct penetration or laceration of the chest wall breaching the parietal pleura, or esophageal perforation that allows air to escape into the and subsequently dissect into the pleural space. In cases of spontaneous pneumothorax, the rupture often involves fragile subpleural blebs or bullae, whose distension and failure can be understood through , which describes the relationship between wall tension (T), transmural pressure (P), and (r) in a spherical structure as P = \frac{2T}{r}. According to this law, for a constant , the internal pressure required to distend or rupture the structure decreases as the radius increases, making larger blebs or bullae more susceptible to rupture under physiological pressures, though small apical blebs in primary spontaneous pneumothorax may fail due to localized high shear forces or reduced wall strength despite the law's prediction. Once air accumulates in the pleural space, the negative equilibrates toward atmospheric levels, removing the gradient that normally counters the lung's intrinsic . This leads to progressive deflation and collapse of the affected , as the elastic fibers in the lung contract unopposed, pulling the visceral pleura away from the parietal pleura. The extent of collapse is proportional to the volume of air in the pleural space and the of the lung tissue, resulting in reduced lung volume and impaired on the affected side. If the air leak persists as a one-way , further accumulation exacerbates the collapse, though the core biophysical process remains the loss of negative pressure enabling .

Physiological consequences

Pneumothorax leads to impaired primarily through the accumulation of air in the pleural , which reduces and causes partial or complete collapse due to . This results in decreased volume, with potentially reduced by up to 33% depending on the size of the pneumothorax. The collapsed regions contribute to ventilation-perfusion (V/Q) mismatch, where is disproportionately reduced compared to , leading to areas of low V/Q ratios and inefficient . Consequently, arterial develops, characterized by a drop in of oxygen (PaO₂), observed in approximately 75% of cases with PaO₂ levels at or below 80 mm Hg, and even lower (≤55 mm Hg) in secondary pneumothorax. Cardiovascular effects arise from the mechanical distortion caused by accumulating pleural air, particularly in moderate to large pneumothoraces. Mediastinal shift toward the unaffected side compresses the vena cava, impeding venous return to the heart and reducing cardiac output. This hemodynamic compromise can exacerbate hypoxemia and lead to tachycardia as the body attempts to maintain perfusion. In severe instances, such as tension pneumothorax, positive intrathoracic pressure builds up, resulting in obstructive shock through further compression of the heart and great vessels, potentially causing profound hypotension and cardiovascular collapse. The body mounts compensatory responses to mitigate these physiological disruptions, including driven by from inadequate CO₂ elimination and stimulation. In prolonged or severe cases, may develop due to retained CO₂, further impairing tissue oxygenation and adding metabolic stress. These responses, while adaptive, can increase the and risk , particularly in patients with underlying lung disease.

Diagnosis

Clinical evaluation

Clinical evaluation of pneumothorax relies on a systematic bedside assessment integrating patient history and to raise diagnostic suspicion prior to imaging. History taking is essential to identify potential etiologies and s. Clinicians should inquire about recent , such as blunt or penetrating chest injuries, which can cause traumatic pneumothorax. Invasive procedures like central venous catheterization, , or lung biopsies are common precipitants of iatrogenic pneumothorax and must be elicited. A detailed history is critical, as use is a primary for spontaneous pneumothorax, particularly in tall, thin young males. Underlying diseases, including (COPD), , or , should also be explored, as they predispose to secondary spontaneous pneumothorax with more severe presentations due to compromised pulmonary reserve. Vital signs provide immediate clues to the severity of pneumothorax. exceeding 100 beats per minute is a frequent finding, reflecting compensatory response to or , while rates over 135 beats per minute raise concern for tension pneumothorax. , often systolic below 90 mmHg, indicates hemodynamic instability in tension cases due to mediastinal shift and reduced venous return. measured by below 90% signals significant , though it may be normal in small pneumothoraces; trending desaturation prompts urgent . Physical examination maneuvers focus on detecting asymmetry and in the affected hemithorax. may reveal reduced chest wall excursion on the ipsilateral side, with and use of accessory muscles in severe cases. assesses for decreased tactile over the pneumothorax area due to air insulating the from vibrations. Percussion typically yields hyperresonance on the affected side from trapped air, though this finding can be subtle or absent in small or obese patients. is key, demonstrating diminished or absent breath sounds unilaterally, with minimal transmission from the contralateral ; in pneumothorax, away from the affected side and jugular venous distention may be evident as late signs. Bedside tests complement the exam by offering rapid, non-invasive insights. Continuous monitoring tracks oxygenation trends, with progressive desaturation indicating expanding pneumothorax or physiology. (ECG) may reveal low-voltage QRS complexes, rightward axis deviation (especially in left-sided pneumothorax), or phasic voltage changes due to cardiac displacement and altered electrical conduction; these findings, while not diagnostic, support suspicion in symptomatic patients.

Chest X-ray

Chest X-ray serves as the initial imaging modality for confirming pneumothorax, particularly after clinical evaluation raises suspicion of the condition. The standard view is the posteroanterior () upright , which allows air to rise to the of the pleural for optimal visualization. In cases of small pneumothoraces, an expiratory phase image can enhance visibility by reducing lung volume and increasing the relative contrast of the air collection against the lung . Key radiographic findings include a thin, white visceral pleural line separated from the parietal pleura by more than 2 cm, with no discernible lung markings in the peripheral lucent zone beyond this line. This line represents the retracted edge of the visceral pleura, and the absence of vascular markings distinguishes pneumothorax from other lucent areas like bullae. The sensitivity of chest for detecting small pneumothoraces (occupying less than 15% of the hemithorax) ranges from 50% to 70%, often lower in or portable films commonly used in settings. In projections, a subtle "deep sulcus sign" may appear as an abnormally deepened and hyperlucent costophrenic angle due to anterior air accumulation, aiding detection of pneumothoraces. Portable chest X-rays in trauma patients can miss up to 30% of pneumothoraces because air layers anteriorly in the supine position, reducing conspicuity. The effective radiation dose from a standard chest X-ray is approximately 0.1 mSv, equivalent to about 10 days of natural background radiation.

Computed tomography

Computed tomography (CT) plays a crucial role in the detailed evaluation of pneumothorax, particularly in cases where initial chest X-ray findings are equivocal or when underlying lung pathology needs assessment. It is indicated for patients with suspected bullae or blebs that may mimic or contribute to pneumothorax, as well as for pre-surgical planning in complex cases involving cystic or interstitial lung disease. CT often follows chest X-ray for initial screening when further clarification is required. Key findings on include precise measurement of pneumothorax size, typically assessed by the interpleural at the level of the hilum, where a greater than 2 indicates a large pneumothorax often requiring intervention based on symptoms. also excels at identifying blebs or bullae, which are subpleural air-filled spaces greater than 1 that can rupture and cause pneumothorax, aiding in distinguishing them from the pneumothorax itself. In addition, can delineate the extent of collapse and detect associated abnormalities such as pleural adhesions or underlying . Different protocols are employed based on clinical suspicion. High-resolution (HRCT), with thin-slice imaging (1-2 ), is particularly useful for evaluating interstitial lung diseases that predispose to secondary spontaneous pneumothorax, such as or Birt-Hogg-Dubé syndrome, by revealing characteristic cystic patterns. Contrast-enhanced is indicated in traumatic pneumothorax to assess for vascular injuries, including active or pseudoaneurysms, which may complicate management. The advantages of include its high of 95-100% for detecting pneumothorax, making it the gold standard for confirming small or cases. It identifies approximately 20% more small pneumothoraces than chest alone, which is critical in or patients where X-ray drops below 50%. However, the effective dose is approximately 7 mSv, higher than the 0.1 mSv of a standard chest , necessitating judicious use.

Ultrasound

Point-of-care ultrasound (POCUS) has emerged as a rapid and effective tool for detecting pneumothorax at the bedside, particularly in and settings where timely is critical. Performed using a high-frequency linear (typically 5–13 MHz), the involves placing the longitudinally along the or in intercostal spaces, starting from the anterior chest (second to fourth intercostal spaces, mid-clavicular line) in patients to assess the pleural line. The absence of "lung sliding"—the normal to-and-fro movement of the visceral pleura against the parietal pleura during —strongly suggests pneumothorax, with a negative predictive value of 99.2–100% when sliding is present. This technique allows for real-time evaluation without the need for patient transport, making it ideal following clinical suspicion of pneumothorax. Key sonographic signs of pneumothorax include the "stratosphere" or "barcode" sign on M-mode imaging, characterized by parallel horizontal lines indicating a stationary pleural line without respiratory variation. A-lines, repetitive horizontal artifacts from the pleura, are typically present, while B-lines (vertical comet-tail artifacts extending to the probe) are absent, further supporting the diagnosis. The "lung point," where sliding transitions to absence, serves as a confirmatory sign with 100% specificity for pneumothorax and aids in estimating its extent. These findings are best visualized in the least dependent lung regions, as air rises anteriorly in patients. Meta-analyses report sensitivity for pneumothorax detection ranging from 78% to 99%, approaching 90–94% in and contexts, with specificity consistently at 98–100%. In comparison, supine chest sensitivity is lower, often 50–70% in acute settings due to positioning limitations. excels at identifying occult pneumothoraces, detecting 30–55% of cases missed by initial supine radiographs. The primary advantages of ultrasound include its portability for immediate use in trauma bays, absence of ionizing radiation, and short examination time (2–3 minutes), enabling faster intervention in unstable patients compared to radiographic alternatives. These attributes contribute to its widespread adoption in point-of-care protocols, enhancing diagnostic accuracy without added risk.

Treatment

Supplemental oxygen and observation

Supplemental oxygen and observation are the initial non-interventional approaches for managing small, stable pneumothoraces, particularly primary spontaneous cases measuring less than 2 cm at the hilum or less than 3 cm at the apex on imaging, in asymptomatic or minimally symptomatic patients without underlying lung disease or hemodynamic instability. This conservative strategy is suitable for adults and older children who maintain adequate oxygenation and show no progression of respiratory distress, allowing for spontaneous resolution in approximately 50-70% of instances without invasive intervention. In neonates, it applies to small (<2-3 cm), stable cases in term or late preterm infants. The mechanism underlying accelerated resolution with supplemental oxygen involves , where high concentrations of oxygen (typically 90-100% FiO₂ via for short periods) reduce the partial pressure of nitrogen in the alveoli, creating a gradient that promotes faster of pleural air compared to room air. This process can increase the resorption rate up to fourfold, from about 1.25% of the pneumothorax volume per day on room air to approximately 5% per day with , though clinical studies show variable impacts on resolution time depending on size and patient factors. Resolution typically occurs over 2-4 weeks in adults. Management involves close monitoring, including serial clinical assessments for signs of respiratory distress every 4-6 hours, continuous , and repeat chest X-rays to track pneumothorax size and lung re-expansion. is advised to minimize activity, and analgesia is provided for discomfort, with intervention thresholds for deterioration such as increasing oxygen needs. Recent guidelines support this approach as effective for cases.

Needle aspiration and decompression

Needle aspiration and serve as immediate interventions to evacuate air from the pleural space in cases of symptomatic pneumothorax, particularly when tension physiology is present or for initial management of primary spontaneous pneumothorax (). This procedure aims to relieve pressure on the and restore hemodynamic by creating a temporary pathway for air release. The involves selecting a large-bore needle, typically 14-16 , to ensure effective . For tension pneumothorax, the needle is inserted over the superior edge of the rib in the second at the midclavicular line, advancing until a rush of air is heard or felt, confirming entry into the pleural space. In non-tension cases, such as symptomatic , uses a three-way stopcock attached to a syringe for active air withdrawal until resistance is met or the lung re-expands. Tension pneumothorax represents the primary indication for emergent needle decompression due to its life-threatening compromise of cardiac output and ventilation. Success rates for needle in PSP range from 50% to 70%, with immediate in about 60-70% of cases, though often necessitates further . For tension pneumothorax, the procedure provides rapid hemodynamic restoration, typically within seconds of air release. Potential complications include , which occurs due to air tracking into soft tissues during insertion, and re-expansion , a rare event affecting less than 1% of cases following rapid lung re-inflation. The British Thoracic Society guidelines recommend needle aspiration as the first-line intervention for symptomatic with a rim of air greater than 2 cm on imaging, prioritizing it over immediate tube drainage in stable patients to minimize invasiveness.

Chest tube insertion

insertion, also known as tube thoracostomy, serves as the definitive treatment for draining large, recurrent, or symptomatic pneumothoraces that do not resolve with less invasive methods such as needle aspiration. It is particularly indicated for cases of failed needle aspiration, secondary spontaneous pneumothorax (e.g., due to underlying lung disease), traumatic pneumothorax, or tension pneumothorax requiring sustained drainage. The procedure involves placing a chest tube, typically sized 16 to 24 French (F), through a small incision in the fourth or fifth intercostal space along the anterior axillary line to target the apical region of the pleural space effectively. After local anesthesia and incision, blunt dissection with a finger (digital exploration) ensures safe entry into the pleural cavity, breaking any adhesions, followed by tube advancement directed superiorly and anteriorly. The tube is secured with sutures and connected to a drainage system featuring an underwater seal to allow one-way air evacuation while preventing atmospheric re-entry; suction may be applied if needed to facilitate lung re-expansion. For smaller or less complex pneumothoraces, digital exploration alone can sometimes suffice without full tube placement, though this is less common for definitive management. As an alternative to traditional large-bore tubes, smaller pigtail catheters (8 to 14 F) can be inserted using a , offering similar efficacy for simple pneumothoraces with reduced patient discomfort and complication risk. Common complications include infection (such as , occurring in approximately 5% of cases), tube malposition (reported in 10 to 20% of insertions, often leading to inadequate drainage), and persistent air leak due to ongoing pleural injury. Other risks encompass bleeding, tissue injury during insertion, and re-expansion , emphasizing the need for guidance to minimize errors. The is typically left in place for an average of 2 to 5 days, until radiographic evidence shows re-expansion, air leak cessation, and minimal pleural fluid output (less than 100 to 200 mL per 24 hours). Removal involves clamping the tube briefly to confirm stability, followed by gentle extraction under sterile conditions.

and surgical interventions

Pleurodesis is a procedure aimed at preventing recurrent pneumothorax by inducing adhesion between the visceral and parietal pleura to obliterate the pleural space. It is typically considered after initial management with drainage, particularly for patients at high risk of recurrence. Methods include chemical and mechanical approaches, with chemical pleurodesis involving the instillation of sclerosing agents such as talc or doxycycline through an intercostal chest tube. Talc slurry achieves success rates of 80% to 95% in preventing recurrence, while doxycycline demonstrates approximately 80% efficacy. Mechanical pleurodesis, often performed via pleural abrasion, is commonly integrated into surgical procedures to promote fibrosis and adhesion. Surgical interventions for recurrent pneumothorax focus on repairing underlying defects and preventing further episodes, with (VATS) serving as the preferred minimally invasive technique. During VATS, bullectomy or blebectomy is conducted to excise emphysematous blebs or bullae, combined with to achieve recurrence prevention in over 95% of cases, based on reported long-term recurrence rates of around 5%. Open thoracotomy is rarely utilized today due to higher morbidity, reserved for cases where VATS is not feasible, such as complex or prior surgical adhesions. Indications for or surgery include recurrent primary spontaneous pneumothorax after more than one episode, or any occurrence of secondary spontaneous pneumothorax, which carries a higher need for intervention due to underlying lung disease. Timing is generally after the first recurrence for primary cases in high-risk patients, such as those in demanding occupations, while secondary cases may warrant earlier definitive treatment to mitigate complications from comorbidities. Complications of these interventions include significant pain, particularly with chemical , necessitating adequate analgesia, and infections such as occurring in 2% to 5% of cases. VATS offers faster recovery with hospital stays of 1 to 3 days compared to 5 to 7 days for open , reducing overall postoperative morbidity.

Aftercare and management in neonates

In neonates, management after treatment for pneumothorax emphasizes close monitoring due to their physiological instability, with a low threshold for insertion even for small pneumothoraces if the is symptomatic, on , or shows signs of respiratory compromise, as delays can lead to rapid . therapy is often integrated into aftercare, particularly in preterm infants with respiratory distress syndrome, to improve and reduce the risk of recurrent air leaks, with administration via endotracheal tube improving oxygenation and potentially shortening ventilation duration. For refractory cases unresponsive to standard interventions, (ECMO) may be employed to support gas exchange while allowing lung rest and resolution of the pneumothorax. A 2021 retrospective study by Andersson et al. in the post-surfactant era demonstrated that a conservative approach is viable for stable neonates, with 84% resolving without invasive intervention such as or drainage, highlighting the potential for in cases. Long-term follow-up in preterm neonates who experienced pneumothorax is essential to monitor for , a chronic condition associated with increased risk following air leak syndromes, involving serial assessments of respiratory status and to guide supportive care.

Prognosis and prevention

Prognosis

The prognosis of pneumothorax varies significantly depending on its type, underlying causes, and timeliness of intervention. For primary spontaneous pneumothorax (PSP), which occurs in individuals without apparent lung disease, mortality is exceedingly low, with rates reported at approximately 1.7% overall and as rare as 1.26 per million annually among men. Survival approaches 99% with appropriate management, reflecting the condition's generally benign course in young, otherwise healthy patients. Recurrence risk remains a key concern, with rates estimated at 30% within five years following the initial episode, though this can be mitigated to 0-15.8% with surgical interventions such as (VATS). In contrast, secondary spontaneous pneumothorax (SSP), associated with underlying lung conditions like (COPD), carries a more guarded outlook. Survival rates range from 80% to 95%, but in-hospital mortality can reach 4.6%, escalating to 1-16% specifically in COPD patients due to compromised respiratory reserve. Recurrence is notably higher, affecting up to 43-50% of cases within five years, underscoring the influence of parenchymal damage. Successful interventions, such as insertion, substantially improve outcomes by promoting lung re-expansion and reducing immediate risks. Tension pneumothorax, a characterized by progressive cardiopulmonary compromise, has a dire if untreated, with near-100% mortality from cardiovascular collapse. Prompt , however, yields excellent results, limiting mortality to under 5% and enabling full recovery in the majority of cases. Several factors adversely affect across pneumothorax types. Advanced age over 50 years correlates with higher mortality and recurrence, often due to comorbid conditions and reduced physiological reserve. exacerbates outcomes by increasing recurrence risk and impairing healing, with studies showing it as an independent predictor of poorer long-term results. With timely , full re-expansion occurs in approximately 95% of cases, highlighting the importance of early in optimizing recovery.

Prevention

Prevention of pneumothorax involves lifestyle modifications and clinical interventions tailored to risk factors and underlying conditions. is a key lifestyle measure, as continued smoking increases the risk of primary spontaneous pneumothorax recurrence, while quitting has been associated with a four-fold reduction in recurrence risk. Individuals who have experienced a pneumothorax should avoid indefinitely due to the high risk of recurrence under pressure changes, even after surgical repair. Clinical strategies for high-risk patients include prophylactic surgery, such as (VATS) to resect blebs or bullae, particularly in cases of primary spontaneous pneumothorax where imaging reveals subpleural abnormalities in tall, thin males who are prone to recurrence. In mechanically ventilated patients, low ventilation (typically 6 mL/kg ideal body weight) limits and reduces the incidence of ventilator-associated pneumothorax to approximately 10 percent. For secondary spontaneous pneumothorax, optimizing management of underlying diseases is essential; in (COPD), regular use of inhaled bronchodilators improves as part of standard pharmacological therapy. Patients with should receive comprehensive pulmonary care to manage lung complications that may predispose to pneumothorax. In neonates, antenatal administration of corticosteroids to mothers at risk of preterm accelerates fetal maturation and reduces the incidence of air leak syndromes, including pneumothorax, by up to 50 percent when combined with . Gentle protocols, emphasizing low tidal volumes and synchronized modes, further decrease pneumothorax rates in preterm infants by minimizing volutrauma.

Epidemiology

Incidence and prevalence

Pneumothorax incidence varies by etiology, with spontaneous forms being the most studied globally. The overall incidence of spontaneous pneumothorax is estimated at 18–28 cases per 100,000 population annually in males and 1.2–6 cases per 100,000 in females, reflecting a higher occurrence in men due to factors like prevalence and anatomical differences. These rates are derived from population-based studies across multiple regions, including and , where data collection from hospital admissions provides consistent benchmarks. Traumatic pneumothorax, resulting from blunt or penetrating chest injuries, has an estimated annual incidence of approximately 81 cases per 100,000 in populations with moderate trauma exposure, though rates can escalate in high-trauma urban or conflict zones. Primary spontaneous pneumothorax (PSP), occurring without underlying lung disease, exhibits a peak incidence in young adulthood, typically between 20 and 30 years of age, with age-specific rates reaching up to 16 cases per 100,000 in the 16–20 age group in some cohorts. In contrast, secondary spontaneous pneumothorax (SSP), associated with preexisting pulmonary conditions such as , shows elevated rates in older individuals, particularly in the 50–70 age range, where underlying or contributes to vulnerability peaking around 60–65 years. Neonatal pneumothorax, a subset often linked to respiratory distress in newborns, affects 1–2% of term births and up to 10% in preterm infants requiring intensive care. Epidemiological trends for pneumothorax have remained largely stable over recent decades in developed regions, with no significant long-term increases in spontaneous cases per population-based analyses from 2017 to 2023. However, during the COVID-19 pandemic, cases linked to mechanical ventilation in intensive care units rose notably, with pneumothorax occurring in up to 14% of intubated COVID-19 patients compared to 2.9% in non-COVID ventilated cohorts, reflecting heightened barotrauma risks from prolonged support. Post-pandemic, rates have reverted toward pre-2020 baselines, though sustained vigilance is recommended for ventilator-associated incidents.

Risk factors and demographics

Pneumothorax exhibits a marked predominance, with a male-to-female of approximately 6:1, particularly evident in cases of primary spontaneous pneumothorax among younger adults. This skew is attributed to anatomical and hormonal factors influencing structure and bleb formation in males. Modifiable risk factors play a significant role in pneumothorax development. substantially elevates the , increasing the likelihood of a first spontaneous pneumothorax by up to 22-fold in men and 9-fold in women, with the effect proportional to the intensity and duration of use. Additionally, shortly after removal for pneumothorax carries a risk of gas in the pleural due to changes, potentially leading to recurrence; guidelines recommend waiting 2-3 weeks post-drainage to mitigate this. Non-modifiable risks include genetic and structural factors. A family history of disorders, such as , confers an elevated lifetime risk of spontaneous pneumothorax estimated at around 10%, due to weakened elastic fibers in the lung tissue. Thoracic deformities, including , are associated with increased incidence of primary spontaneous pneumothorax, as the altered chest wall mechanics may promote subpleural bleb rupture. Certain occupational and recreational groups face heightened risks from or pressure changes. are particularly susceptible to traumatic pneumothorax, which accounts for 3-4% of fatalities in casualties, often from penetrating injuries or effects. divers experience barotrauma-related pneumothorax resulting from lung overexpansion during ascent if air is not properly exhaled.

History and etymology

History

The recognition of pneumothorax as a distinct medical condition dates back to the early , when Jean-Marc Gaspard Itard, a student of , first identified it as a pathological entity in 1803 and coined the term to describe air in the . Laennec provided a more comprehensive clinical description in 1819, outlining its symptoms and auscultatory findings in patients with pulmonary tuberculosis, which was a common underlying cause at the time. These early observations laid the foundation for understanding pneumothorax as a complication of disease rather than merely a postmortem finding. In the late , the concept evolved from passive observation to active therapeutic intervention, particularly for . Italian physician Carlo Forlanini pioneered artificial pneumothorax in 1882, proposing the intentional introduction of air into the pleural space to collapse the affected and promote rest and healing, based on experiments with animal models and clinical trials. This method gained traction in the early as a standard treatment for pulmonary before the advent of antibiotics, with refinements in technique allowing for repeated insufflations to maintain collapse. The 20th century saw significant advances driven by wartime experiences, particularly in managing traumatic pneumothorax. During , military surgeons recognized tension pneumothorax as a frequent and lethal complication of penetrating chest wounds, often resulting from air leakage into the pleural space under pressure, leading to improved protocols for immediate decompression using needles or tubes to restore . Following the (1950–1953), chest tube thoracostomy became standardized for treating and pneumothorax, with technological improvements in tube design and closed drainage systems reducing complications and establishing it as the cornerstone of care for traumatic cases. In the , treatment shifted toward minimally invasive and evidence-based approaches. (VATS) emerged in the as a preferred method for recurrent spontaneous pneumothorax, enabling bullectomy and through small incisions with lower morbidity than open . The British Thoracic Society () issued comprehensive guidelines in 2003 for managing spontaneous pneumothorax, emphasizing observation for small cases and intervention for larger or symptomatic ones, which were updated in 2010 to incorporate advances in imaging and ambulatory management, and further in 2023 as part of the Pleural Disease Guideline.

Etymology

The term pneumothorax derives from the words pneuma (πνεῦμα), meaning "air" or "breath," and thorax (θώραξ), meaning "chest" or "breastplate," literally denoting air within the chest cavity. This nomenclature was first introduced in by the French physician Jean-Marc Gaspard Itard in 1803, who used it to describe the pathological accumulation of air in the pleural space. Early in its usage, "pneumothorax" often referred to artificial pneumothorax, a deliberate therapeutic procedure developed by Italian physician Carlo Forlanini in 1882 to treat pulmonary by collapsing the affected lung through air injection into the , thereby promoting rest and healing. As tuberculosis therapy declined with the advent of antibiotics in the mid-20th century, the term evolved to encompass pathological subtypes, including pneumothorax simplex—a designation for uncomplicated spontaneous pneumothorax in healthy individuals without evident cause, proposed in early 20th-century observations of non-tuberculous cases. Similarly, tension pneumothorax emerged to characterize the progressive buildup of air under positive pressure in the pleural space, a life-threatening variant recognized through mid-20th-century advancements in and defined by exceeding atmospheric levels throughout the respiratory cycle. Related compound terms include , incorporating the Greek prefix hydro- (ὕδωρ, meaning "water" or "fluid") to indicate the coexistence of air and , and hemopneumothorax, prefixed with hemo- (from haima, αἷμα, meaning "blood") to describe air accompanied by . These variants adhere to classical Greco-Latin medical , building on the root pneumothorax to specify additional pathological elements.

Other animals

In companion animals

Pneumothorax in companion animals, primarily and , is a condition characterized by the accumulation of air in the pleural , leading to collapse and potential respiratory compromise. It is relatively uncommon in small animal veterinary practice, though traumatic cases are more frequent than spontaneous ones. Deep-chested breeds such as Siberian Huskies are predisposed to primary spontaneous pneumothorax due to the rupture of pulmonary bullae or blebs. The most common cause of pneumothorax in dogs and cats is , accounting for up to 50% of cases involving thoracic injuries, often from accidents, bite wounds, or penetrating injuries like those from "hit-by-car" incidents. Secondary causes include neoplasia, which is more prevalent in dogs, and pyothorax or infectious processes, while in cats, underlying inflammatory lung diseases such as feline asthma contribute to spontaneous forms. pneumothorax can arise from diaphragmatic hernias, typically secondary to , exacerbating the condition by shifting mediastinal structures. The involves air leakage into the pleural space, causing similar to that in humans, which impairs and can lead to if untreated. Diagnosis relies on clinical signs such as dyspnea, , and diminished sounds, confirmed by thoracic radiographs showing visceral pleural lines or lobe collapse, and thoracic for rapid bedside assessment in emergencies. Advanced imaging like may identify underlying bullae in spontaneous cases. Treatment begins with stabilization using supplemental oxygen to alleviate , followed by thoracocentesis to evacuate air from the pleural space, a procedure that mirrors emergency management and provides immediate relief in most cases. For persistent or spontaneous pneumothorax, indwelling thoracostomy tubes or surgical intervention, such as bullectomy or , is often necessary, particularly in dogs to prevent recurrence. Prognosis is generally favorable with prompt veterinary , with survival rates exceeding 85% in traumatic pneumothorax cases and up to 90% in surgically managed spontaneous cases in , where recurrence is low (less than 10%) following resection of affected tissue. In , outcomes are slightly more guarded due to diffuse , with survival around 50-70% depending on the underlying cause, though early thoracocentesis improves chances significantly. Complications like pleural can worsen in chronic cases, but overall, most companion animals recover fully with appropriate care.

In livestock and wildlife

Pneumothorax in species, such as , , and pigs, is typically secondary to underlying pulmonary or , leading to respiratory compromise that requires prompt intervention. In , the condition is frequently linked to , with a retrospective study of 30 cases from 1990 to 2003 identifying this as the primary underlying cause in most instances; affected often presented with dyspnea, reduced production, and abnormal sounds, and treatment involved thoracic with variable success depending on the severity of the concurrent . Management strategies include continuous-flow evacuation systems to resolve air accumulation, particularly in cases associated with acute or , which can prevent fatal respiratory distress if implemented early. In horses, pneumothorax is predominantly traumatic, arising from thoracic wounds, rib fractures, or penetrating injuries such as those from fences or kicks; clinical signs include rapid, shallow breathing and respiratory distress, with diagnosis confirmed via ultrasound or radiography showing air in the pleural space. Treatment focuses on immediate air evacuation through thoracocentesis or indwelling drains, alongside wound management and antibiotics to address secondary pleuritis, as demonstrated in a case of a 10-year-old gelding with a bilateral puncture wound that resolved following rapid intervention to seal the leak and remove accumulated air. In pigs, occurrences are less common but include iatrogenic cases during mechanical ventilation under anesthesia, as seen in two Vietnamese potbellied pigs where positive pressure led to air leakage into the pleural space, necessitating immediate decompression. Spontaneous pneumothorax has also been documented in companion breeds like Kunekune pigs, attributed to rupture of pulmonary bullae, with successful resolution via thoracotomy and lung resection in a reported three-month-old case. Reports of pneumothorax in wildlife are infrequent but highlight traumatic etiologies in free-ranging or rescued animals. In Korean water deer (Hydropotes inermis argyropus), a common wild species in Korea, traumatic pneumothorax from vehicular collisions or falls has been successfully treated with chest tube insertion and supportive care, as in a female deer rescued with severe dyspnea that recovered fully after air evacuation and monitoring. Similarly, in Florida manatees (Trichechus manatus latirostris), pneumothorax often accompanies boat strikes or entrapment injuries, with conservative management—including buoyancy aids like wetsuits and serial aspirations—leading to resolution in two documented cases without surgical intervention, emphasizing the role of specialized wildlife rehabilitation. These instances underscore the challenges of treating pneumothorax in non-domesticated species, where access to veterinary care and species-specific anatomy influence outcomes.

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