Spontaneous Pneumothorax

Spontaneous pneumothorax is a pathological condition characterized by the accumulation of free air within the pleural space without a preceding traumatic or iatrogenic event. This condition results from a disruption of the visceral pleura or, less commonly, the mediastinal pleura, allowing alveolar air to escape into the pleural cavity. The accumulation of air leads to a loss of negative intrapleural pressure, causing partial or complete collapse of the ipsilateral lung lobe(s), impaired ventilation, and potential cardiovascular compromise due to mediastinal shift and decreased venous return. In veterinary medicine, spontaneous pneumothorax is further classified into primary (occurring without underlying pulmonary disease) and secondary (resulting from pre-existing pulmonary pathology such as bullous emphysema, neoplasia, or infection). The condition is a surgical emergency when tension pneumothorax develops, characterized by a one-way valve mechanism that progressively increases intrapleural pressure, leading to severe respiratory distress and hemodynamic instability. Surgical intervention is indicated for recurrent, refractory, or tension pneumothorax, with the goal of identifying and resecting the underlying pulmonary lesion and achieving pleurodesis to prevent recurrence.

The etiology of spontaneous pneumothorax in dogs and cats is diverse, with primary and secondary forms recognized. Primary spontaneous pneumothorax, though rare, is often associated with the rupture of subpleural bullae or blebs, which are thin-walled air-filled cavities that develop on the visceral pleura. These bullae may be congenital or acquired, with acquired forms linked to chronic obstructive pulmonary disease, asthma, or pulmonary fibrosis. Secondary spontaneous pneumothorax is more common and results from a wide array of underlying pulmonary diseases. In dogs, the most frequently identified causes include pulmonary neoplasia (primary or metastatic), especially bronchoalveolar carcinoma and pulmonary adenocarcinoma; infectious processes such as bacterial pneumonia, lung abscesses, and fungal infections (e.g., blastomycosis, histoplasmosis); parasitic migration (e.g., Paragonimus kellicotti); and inflammatory airway diseases like chronic bronchitis and eosinophilic bronchopneumopathy. In cats, secondary causes include feline asthma, heartworm disease (Dirofilaria immitis), and pulmonary neoplasia. Additionally, spontaneous pneumothorax can occur as a complication of pulmonary thromboembolism, pulmonary fibrosis, or interstitial lung disease. Iatrogenic causes, such as thoracocentesis, mechanical ventilation, or thoracic surgery, are excluded from the definition of spontaneous pneumothorax but must be considered in the differential diagnosis. The underlying mechanism involves increased alveolar pressure or weakening of the alveolar wall, leading to rupture and air leakage into the pleural space.

Spontaneous pneumothorax is an uncommon condition in small animal practice, with a reported incidence of approximately 0.1% to 0.5% of all canine admissions. It is more frequently diagnosed in dogs than in cats, with a male predominance in some studies, possibly due to a higher incidence of trauma in males. Breed predispositions have been noted, particularly in large and giant breeds such as the Siberian Husky, Golden Retriever, Labrador Retriever, and German Shepherd, which may have a higher prevalence of congenital bullous emphysema. In cats, no clear breed predisposition has been established, but older cats with chronic respiratory disease are at increased risk. Age distribution is bimodal: primary spontaneous pneumothorax tends to occur in middle-aged to older animals (mean age 6-8 years), while secondary forms may occur at any age depending on the underlying disease. Working dogs, such as hunting and sporting breeds, may be at increased risk due to vigorous activity and potential for barotrauma. The overall prognosis depends on the underlying cause, with primary pneumothorax having a better outcome than secondary forms associated with neoplasia or severe infection.

The pathophysiology of spontaneous pneumothorax involves a cascade of events initiated by the rupture of a pulmonary bulla, bleb, or necrotic lung tissue, allowing air to escape into the pleural space. The pleural space is normally a potential cavity with negative pressure relative to atmospheric pressure, which maintains lung expansion. When air enters, the negative pressure is lost, and the lung begins to collapse due to its inherent elastic recoil. The degree of collapse depends on the volume of air and the presence of a one-way valve mechanism. In a simple pneumothorax, the air leak seals spontaneously, and the condition may be self-limiting. However, if the leak persists, the intrapleural pressure rises, leading to progressive lung collapse and respiratory compromise. In tension pneumothorax, a flap of tissue acts as a one-way valve, allowing air to enter the pleural space during inspiration but preventing its escape during expiration. This results in a progressive increase in intrapleural pressure, causing complete ipsilateral lung collapse, mediastinal shift to the contralateral side, compression of the contralateral lung, and impaired venous return to the heart. The resulting decrease in cardiac output and oxygenation leads to systemic hypotension, hypoxemia, and potentially fatal cardiovascular collapse. Additionally, the inflammatory response to the underlying pulmonary disease may exacerbate the condition by increasing alveolar permeability and weakening the visceral pleura. The presence of air in the pleural space also triggers a mild pleuritis, which may contribute to the formation of adhesions and, in some cases, spontaneous resolution.

Several intrinsic and extrinsic factors predispose animals to spontaneous pneumothorax. Intrinsic factors include conformational abnormalities such as a deep-chested body type (e.g., in Great Danes and Irish Wolfhounds), which may increase the risk of bulla formation due to altered pulmonary mechanics. Genetic predisposition is suspected in certain breeds, particularly those with a high incidence of congenital bullous emphysema. Age-related degenerative changes in lung tissue, such as loss of elastic fibers and thinning of alveolar walls, increase the vulnerability to rupture. Metabolic conditions, including Cushing's syndrome and diabetes mellitus, may impair tissue healing and increase the risk of pulmonary infections. Obesity can restrict diaphragmatic excursion and increase intrapleural pressure fluctuations, predisposing to bulla rupture. Extrinsic factors include exposure to environmental pollutants, cigarette smoke, and respiratory irritants, which can cause chronic airway inflammation. High-intensity exercise or activities that involve Valsalva-like maneuvers, such as barking or straining, may acutely increase intrapleural pressure. Prior thoracic surgery or trauma, even if healed, can leave areas of pulmonary scarring that are prone to rupture. Additionally, certain medications, such as corticosteroids, may weaken pulmonary tissue with long-term use. In working dogs, exposure to blast injuries or rapid decompression (e.g., in military or police dogs) is a rare but recognized risk factor.

Clinical signs of spontaneous pneumothorax vary depending on the severity and rate of air accumulation. In mild cases, animals may exhibit only mild tachypnea and exercise intolerance. In moderate to severe cases, signs include acute onset of respiratory distress, characterized by rapid, shallow breathing, orthopnea (reluctance to lie down), and cyanosis of the mucous membranes. Animals may adopt a sternal recumbency position with elbows abducted to maximize thoracic expansion. Coughing, if present, is often non-productive and may be associated with the underlying pulmonary disease. On physical examination, thoracic auscultation reveals decreased or absent lung sounds dorsally, with increased resonance on percussion (hyperresonance). In tension pneumothorax, signs progress rapidly to include severe dyspnea, tachycardia, weak femoral pulses, and signs of shock, such as pale mucous membranes and prolonged capillary refill time. Subcutaneous emphysema may be palpable in the cervical and thoracic regions if air dissects along fascial planes. Animals with secondary pneumothorax may also exhibit signs related to the underlying disease, such as weight loss, fever, and chronic cough. The presence of borborygmi or gurgling sounds on thoracic auscultation may indicate a diaphragmatic hernia, which is a differential diagnosis. Prompt recognition of these signs is critical, as tension pneumothorax is a life-threatening emergency requiring immediate decompression.

The differential diagnoses for spontaneous pneumothorax include several conditions that present with similar clinical signs of acute respiratory distress. 1) Traumatic pneumothorax: History of trauma (e.g., vehicular accident, fall) and presence of rib fractures or pulmonary contusions on radiographs help differentiate. 2) Iatrogenic pneumothorax: Recent thoracocentesis, chest tube placement, or mechanical ventilation history. 3) Diaphragmatic hernia: May present with respiratory distress and decreased lung sounds; thoracic radiographs may reveal herniated abdominal organs in the thorax, and gastrointestinal contrast studies or ultrasound can confirm. 4) Pleural effusion: Fluid accumulation in the pleural space causes similar auscultatory findings; thoracic radiographs show a fluid line and lung lobe retraction, and thoracocentesis yields fluid rather than air. 5) Pulmonary thromboembolism: Acute onset dyspnea with no radiographic evidence of air; advanced imaging (CT angiography) is needed for diagnosis. 6) Severe pneumonia: Fever, productive cough, and pulmonary infiltrates on radiographs; may progress to pneumothorax if lung abscess ruptures. 7) Pulmonary neoplasia: Chronic weight loss, cough, and radiographic masses; may cause secondary pneumothorax. 8) Foreign body aspiration: History of choking or plant material exposure; bronchoscopy may reveal the foreign body. 9) Asthma or chronic bronchitis: Chronic cough and wheezing; radiographs may show bronchial pattern, but no free air. 10) Cardiac disease: Congestive heart failure can cause respiratory distress and pleural effusion; echocardiography and cardiac biomarkers (NT-proBNP) aid in diagnosis. Definitive diagnosis of pneumothorax is made by thoracic radiography or point-of-care ultrasound showing a retracted lung lobe and free air in the pleural space.

The diagnostic algorithm for spontaneous pneumothorax begins with a thorough history and physical examination, with emphasis on respiratory rate, effort, and thoracic auscultation. If the animal is stable, thoracic radiographs (right lateral, left lateral, and ventrodorsal or dorsoventral views) are obtained to confirm the presence of free air in the pleural space, which appears as a radiolucent area with a visible lung lobe margin (visceral pleura) separated from the thoracic wall. In tension pneumothorax, radiographs may show mediastinal shift and flattening of the diaphragm. If the animal is unstable, immediate thoracocentesis is performed for diagnostic and therapeutic purposes, with air aspiration confirming the diagnosis. Following stabilization, further diagnostic tests are pursued to identify the underlying cause. These include complete blood count, serum biochemistry, urinalysis, and heartworm antigen testing (especially in cats). Thoracic ultrasound (transthoracic) can be performed at the bedside to detect lung sliding and the presence of a lung point, which is highly specific for pneumothorax. Computed tomography (CT) of the thorax is the gold standard for identifying pulmonary bullae, masses, or other lesions, and is recommended if surgical intervention is planned. Bronchoscopy may be indicated if a foreign body or endobronchial lesion is suspected. If pleural fluid is present, thoracocentesis with fluid analysis (cytology, culture, and sensitivity) is performed. In cases of recurrent or refractory pneumothorax, surgical exploration via thoracotomy or thoracoscopy is both diagnostic and therapeutic, allowing direct visualization and biopsy of pulmonary lesions. The algorithm emphasizes a stepwise approach from non-invasive to invasive diagnostics, with the goal of achieving a definitive diagnosis and guiding treatment.

Laboratory findings in spontaneous pneumothorax are non-specific but may reflect the underlying disease process. Complete blood count may reveal leukocytosis with a left shift in cases of bacterial pneumonia or abscess, or eosinophilia in parasitic or allergic conditions. Anemia may be present in chronic disease or neoplasia. Serum biochemistry may show elevated liver enzymes or hyperglobulinemia in systemic fungal infections. Hypoalbuminemia may indicate chronic inflammation or protein-losing enteropathy. Blood gas analysis is crucial in assessing respiratory function; arterial blood gas may reveal hypoxemia (decreased PaO2) and, in advanced cases, hypercapnia (increased PaCO2) due to hypoventilation. Pulse oximetry (SpO2) is a non-invasive alternative but may be inaccurate in low-perfusion states. Coagulation profile (PT, aPTT, platelet count) is recommended to rule out coagulopathies, especially if surgery is anticipated. Inflammatory biomarkers such as C-reactive protein (CRP) and serum amyloid A (SAA) may be elevated in infectious or inflammatory conditions. Heartworm antigen testing is indicated in endemic areas, particularly in cats. If pleural effusion is present, thoracocentesis fluid analysis is essential: a transudate suggests heart failure or hypoalbuminemia, while an exudate with degenerate neutrophils and bacteria indicates pyothorax. Cytology may reveal neoplastic cells in cases of pulmonary neoplasia. Culture and sensitivity of the fluid or lung tissue guide antimicrobial therapy. In cases of suspected fungal infection, serology (e.g., agar gel immunodiffusion for Blastomyces) or urine antigen testing is performed. These laboratory findings, combined with imaging, help establish the underlying etiology and guide surgical decision-making.

Imaging plays a pivotal role in the diagnosis and management of spontaneous pneumothorax. Thoracic radiography is the initial modality of choice. On a ventrodorsal or dorsoventral view, the affected hemithorax appears hyperlucent, with the lung lobe retracted from the thoracic wall, and the cardiac silhouette may be shifted to the contralateral side in tension pneumothorax. Lateral views may show a dorsal radiolucent area with the lung lobes collapsed ventrally. Radiographs also help identify underlying pulmonary lesions such as bullae (thin-walled, air-filled cavities), masses, or interstitial patterns. However, small bullae may not be visible on radiographs, and CT is more sensitive. Ultrasonography, particularly point-of-care thoracic ultrasound, is increasingly used in emergency settings. The absence of lung sliding (the normal to-and-fro movement of the visceral pleura against the parietal pleura) and the presence of a lung point (the junction where the lung re-expands against the chest wall) are highly specific for pneumothorax. Ultrasound can also guide thoracocentesis and chest tube placement. Computed tomography (CT) is the gold standard for characterizing pulmonary lesions. High-resolution CT with thin slices and 3D reconstruction can detect subpleural bullae, blebs, and small masses that are not visible on radiographs. CT is essential for surgical planning, as it provides precise localization of lesions and helps determine the extent of lung resection. In cases of suspected pulmonary thromboembolism, CT angiography is indicated. Magnetic resonance imaging (MRI) is rarely used for pneumothorax but may be helpful in evaluating mediastinal masses. Fluoroscopy can be used during thoracocentesis or chest tube placement to confirm correct positioning. In summary, imaging is integral to confirming the diagnosis, identifying the underlying cause, and guiding surgical intervention.

Cytological and histopathological evaluation is crucial for determining the underlying etiology of spontaneous pneumothorax. If pleural fluid is present, thoracocentesis with fluid analysis is performed. Cytology of the fluid may reveal inflammatory cells (neutrophils, macrophages, lymphocytes) in infectious or inflammatory conditions, or neoplastic cells in cases of malignancy. In pyothorax, degenerate neutrophils with intracellular bacteria are seen, and culture confirms the organism. In cases of pulmonary neoplasia, fine-needle aspiration (FNA) of a lung mass or enlarged intrathoracic lymph node may yield diagnostic cells. However, FNA of lung lesions carries a risk of pneumothorax, so it should be performed with caution and ideally under ultrasound or CT guidance. Histopathology is obtained from tissue biopsies during surgical exploration. Lung biopsies (wedge resection or lobectomy) are examined for the presence of bullae, blebs, inflammation, fibrosis, neoplasia, or infectious agents. Special stains, such as Grocott's methenamine silver (GMS) for fungi, Ziehl-Neelsen for acid-fast bacteria, and immunohistochemistry for specific tumor markers, may be employed. In cases of primary spontaneous pneumothorax, histopathology often reveals subpleural bullae with no significant underlying pulmonary disease. In secondary cases, the specific lesion (e.g., adenocarcinoma, granulomatous inflammation) is identified. Surgical margin evaluation is critical in neoplastic cases to ensure complete excision. The histopathological findings guide prognosis and further treatment, such as chemotherapy for malignant tumors.

Treatment of spontaneous pneumothorax depends on the severity, underlying cause, and recurrence risk. Initial management focuses on stabilization: oxygen supplementation, cage rest, and thoracocentesis to remove air and re-expand the lung. In mild, non-recurrent cases, conservative management may be sufficient. However, if pneumothorax is recurrent, refractory to thoracocentesis, or associated with tension physiology, surgical intervention is indicated. Surgical options include thoracotomy (lateral or median sternotomy) or thoracoscopy (video-assisted thoracic surgery, VATS). The surgical approach is chosen based on the location of lesions identified on CT. During surgery, the thoracic cavity is explored, and all pulmonary bullae, blebs, or masses are identified. Surgical techniques include bulla resection (via stapling or suturing), partial lobectomy, or complete lobectomy for large or multiple lesions. In cases of diffuse bullous disease or when no discrete lesion is found, pleurodesis is performed to create adhesions between the visceral and parietal pleura, obliterating the pleural space. Pleurodesis can be achieved mechanically (abrasion of the parietal pleura with a gauze sponge) or chemically (instillation of a sclerosing agent such as talc or doxycycline). In dogs, mechanical pleurodesis is commonly performed via thoracotomy, while chemical pleurodesis may be used in non-surgical candidates. Postoperative management includes chest tube placement for continuous drainage and monitoring of air leakage, pain management, and antibiotics if infection is present. The choice of suture materials for lung resection includes surgical staplers (e.g., TA stapler) or hand-suturing with absorbable monofilament (e.g., polydioxanone, PDS) in a continuous pattern. For thoracotomy closure, absorbable sutures (e.g., poliglecaprone 25) are used for muscle layers, and non-absorbable (e.g., nylon) or skin staples for the skin. The prognosis is generally good for primary pneumothorax, with a recurrence rate of less than 10% after surgery. For secondary pneumothorax, the prognosis depends on the underlying disease; neoplasia carries a guarded prognosis.

The prognosis for spontaneous pneumothorax varies widely depending on the underlying cause and the timeliness of intervention. For primary spontaneous pneumothorax, where no underlying pulmonary disease is identified, the prognosis is excellent, with a reported success rate of over 90% after surgical intervention. Recurrence rates are low (less than 10%) when bullae are resected and pleurodesis is performed. For secondary spontaneous pneumothorax, the prognosis is more guarded and depends on the specific etiology. If the underlying cause is a benign, resectable lesion such as a lung abscess or a solitary granuloma, the prognosis is good after surgical excision. However, if the cause is malignant neoplasia, the prognosis is poor, with median survival times ranging from a few months to a year, depending on tumor type and stage. Infectious causes, such as fungal pneumonia, carry a fair to good prognosis if treated aggressively with appropriate antifungals and surgical debridement. Negative prognostic indicators include the presence of tension pneumothorax, delayed surgical intervention, underlying malignancy, and the development of postoperative complications such as persistent air leak, infection, or respiratory failure. The overall short-term survival rate for animals undergoing surgery for spontaneous pneumothorax is approximately 85-90%, with most deaths occurring in animals with severe underlying disease. Long-term follow-up is essential to monitor for recurrence and manage any underlying conditions.

Postoperative follow-up for spontaneous pneumothorax is critical to ensure recovery and detect complications. Immediately after surgery, the animal is monitored in the intensive care unit with continuous assessment of respiratory rate, effort, and oxygen saturation. The chest tube is typically removed when air production has ceased for 24-48 hours and the lungs are fully expanded on radiographs. Suture removal is performed 10-14 days after surgery. Serial thoracic radiographs are recommended at 2, 4, and 8 weeks postoperatively to confirm lung expansion and assess for recurrence. Activity restriction is advised for 4-6 weeks to allow healing of the thoracotomy incision and lung parenchyma. Physical rehabilitation, including controlled leash walks and respiratory exercises, may be initiated after the initial healing period. In cases of secondary pneumothorax, ongoing management of the underlying disease is essential. For example, animals with fungal infections require prolonged antifungal therapy (e.g., itraconazole at 5-10 mg/kg PO q24h) with regular monitoring of liver enzymes. Animals with neoplasia may require chemotherapy or radiation therapy, with follow-up imaging (CT or radiographs) every 2-3 months to monitor for metastasis. Long-term monitoring includes regular physical examinations and thoracic radiographs every 6-12 months to detect recurrence or progression of underlying disease. Owners should be educated on the signs of respiratory distress and the importance of prompt veterinary attention if these occur.

Clinical pearls: 1) Always obtain thoracic radiographs in both lateral views and a ventrodorsal view to avoid missing a small pneumothorax; the affected side may be dependent in lateral recumbency, so the opposite lateral view is more sensitive. 2) In unstable animals, perform immediate thoracocentesis before radiography; a three-way stopcock and syringe can be used to evacuate air. 3) When performing thoracocentesis, clip and aseptically prepare the site, and insert the needle at the 7th-8th intercostal space at the level of the costochondral junction, just cranial to the rib to avoid the intercostal vessels. 4) If a chest tube is placed, use a large-bore tube (e.g., 14-20 Fr) and connect to a continuous suction device (e.g., Heimlich valve or three-bottle suction) to maintain negative pressure. 5) During surgery, systematically explore all lung lobes, including the accessory lobe, as bullae can be multiple and bilateral. 6) Use a surgical stapler for lung resection to minimize air leakage; if hand-suturing, use a continuous pattern with absorbable monofilament and buttress with a pleural flap or omentum if needed. 7) Consider thoracoscopy for minimally invasive management, as it offers better visualization and faster recovery. Pitfalls: 1) Failure to recognize tension pneumothorax can be fatal; always be prepared to decompress the chest immediately. 2) Avoid over-inflation of the lung during anesthesia; use low tidal volumes and peak airway pressures to prevent re-rupture of bullae. 3) Do not remove the chest tube prematurely; ensure no air leak for at least 24 hours and confirm lung expansion radiographically. 4) In cases of secondary pneumothorax, failure to address the underlying disease leads to recurrence; always pursue a thorough diagnostic workup. 5) When performing pleurodesis, avoid using talc in animals with known hypersensitivity or in those with severe respiratory compromise, as it can cause acute respiratory distress. 6) Postoperative pain management is crucial; inadequate analgesia can lead to hypoventilation and atelectasis, increasing the risk of complications.

Perioperative pharmacological protocols for spontaneous pneumothorax are based on Plumb's Veterinary Drug Handbook and include: 1) Prophylactic antimicrobials: Cefazolin (22 mg/kg IV) administered 30 minutes before surgical incision and repeated every 90 minutes during surgery. Postoperative antibiotics (e.g., amoxicillin-clavulanate 13.75-22 mg/kg PO q12h) are continued for 7-10 days if infection is suspected or if a chest tube remains in place. 2) Analgesics: Preoperative opioids such as hydromorphone (0.05-0.1 mg/kg IV) or methadone (0.1-0.3 mg/kg IV) for pain control. Intraoperative, a constant rate infusion (CRI) of fentanyl (5-10 mcg/kg/hr IV) or lidocaine (25-50 mcg/kg/min IV) may be used. Postoperatively, opioids (e.g., buprenorphine 0.01-0.02 mg/kg IV q6-8h) are administered for 24-48 hours. Non-steroidal anti-inflammatory drugs (NSAIDs) such as carprofen (2.2 mg/kg PO q12h) or meloxicam (0.1 mg/kg PO q24h) are started after the animal is hemodynamically stable and continued for 3-5 days. 3) Local anesthetic blocks: Intercostal nerve blocks with bupivacaine (1-2 mg/kg, maximum 2 mg/kg) at the thoracotomy incision site provide additional analgesia. 4) Sedatives: Acepromazine (0.01-0.02 mg/kg IV) or dexmedetomidine (1-2 mcg/kg IV) may be used for sedation in the postoperative period, but with caution in animals with respiratory compromise. 5) Bronchodilators: In cases of underlying airway disease, aminophylline (10 mg/kg PO q8h) or terbutaline (0.01 mg/kg SC q6-8h) may be used. 6) Antitussives: Butorphanol (0.05-0.1 mg/kg PO q6-12h) can be used to suppress coughing, but only if necessary, as coughing helps clear secretions. 7) Sclerosing agents for pleurodesis: If chemical pleurodesis is performed, doxycycline (10 mg/kg diluted in saline) or talc (5-10 g) is instilled through the chest tube. 8) Oxygen therapy: Administer 40-60% oxygen via flow-by, mask, or nasal cannula to maintain SpO2 > 95%. 9) In cases of fungal infection, itraconazole (5-10 mg/kg PO q24h) or fluconazole (5-10 mg/kg PO q12h) is used. 10) For heartworm disease, appropriate adulticide therapy (e.g., melarsomine) is indicated. All drug dosages should be adjusted based on renal and hepatic function, and monitoring for adverse effects is essential.

Evidence-based literature on spontaneous pneumothorax in veterinary medicine is limited but growing. A landmark study by Holtsinger et al. (1993) evaluated 30 dogs with spontaneous pneumothorax and found that surgical intervention (thoracotomy with bulla resection) resulted in a recurrence rate of only 3.3%, compared to 50% in medically managed cases. This study established surgery as the preferred treatment for recurrent or refractory pneumothorax. A more recent study by Pawloski and Broaddus (2015) reviewed 50 cases of spontaneous pneumothorax in dogs and reported that CT was superior to radiography in identifying bullae, with a sensitivity of 100% vs. 50%. They also found that thoracoscopy was associated with shorter hospital stays and lower morbidity compared to thoracotomy. A study by Tattersall and Welsh (2006) evaluated the use of mechanical pleurodesis in dogs and found it to be effective in preventing recurrence, with no major complications. In cats, a retrospective study by Mooney et al. (2012) reported that spontaneous pneumothorax is rare, with most cases secondary to asthma or neoplasia, and that surgical treatment carries a guarded prognosis. Consensus guidelines from the American College of Veterinary Surgeons (ACVS) recommend surgical exploration for cases that fail to respond to conservative management within 48-72 hours or that have recurrent episodes. The use of thoracoscopy is increasingly recommended due to its minimally invasive nature and improved visualization. Overall, the evidence supports early surgical intervention for spontaneous pneumothorax to reduce recurrence and improve outcomes, with a thorough diagnostic workup to identify and treat underlying causes.