Thoracic Cavity

The thoracic cavity is made of 13 pairs of ribs, 13 thoracic vertebrae, and nine sternebrae. The ribs and sternum maintain the shape of the thoracic cavity, which allows expansion of the lungs. The internal and external intercostal muscles connect the ribs together. Muscles that cover the thoracic wall, from inside to outside, include the serratus dorsalis and ventralis, scalenus, external oblique, latissimus dorsi, pectoralis, and cutaneous trunci.

An intercostal nerve, vein, and artery are located caudal to the cranial rib in each intercostal space. The intercostal arteries arise directly from the aorta and anastomose with the internal thoracic arteries. The first intercostal artery, a branch of the costocervical trunk, supplies the first three intercostal arteries. Intercostal veins are drained by the azygos vein, except for the first intercostal vein, which is drained by the costocervical vein.

Lungs

The left lung of dogs and cats is divided into cranial and caudal lobes (Figure 103-1, A). The left cranial lung lobe is divided into a cranial and caudal portion but shares a common lobar bronchus. The right lung is divided into four distinct lobes: cranial, middle, caudal, and accessory (Figure 103-1, B). The accessory lobe passes dorsal to the caudal vena cava and is located medial to the plica vena cava.

The trachea divides into two principle bronchi, which in turn subdivide into lobar bronchi that supply each lung lobe (Figure 103-2). Within each lung lobe, lobar bronchi divide into segmental bronchi that supply bronchopulmonary segments. Dichotomous branching of the airway continues through subsegmental bronchi, terminal bronchioles, and respiratory bronchioles. Respiratory bronchioles give rise to alveolar ducts, alveolar sacs, and pulmonary alveoli.

Pulmonary arteries follow a lobar distribution in close proximity to the cranial dorsal aspect of each bronchus. Bronchial branches of the bronchoesophageal arteries provide oxygenated blood to the airways down to the level of the respiratory bronchioles, where they terminate in capillary beds continuous with the pulmonary arteries. Pulmonary veins course on the caudal and ventral aspect of each bronchus, collecting blood from both the pulmonary and bronchial arteries.

Ventilation

Ventilation is the process of moving air in and out of the alveoli. It requires input from the brain respiratory centers, spinal cord, peripheral nerves, and the respiratory muscles and the presence of negative pressure in the pleural spaces, which allows coupling between the lung and the thoracic wall. Normal resting ventilation is accomplished primarily by the diaphragm during inspiration and elastic recoil during expiration.¹⁰² During inspiration, the diaphragm contracts, pulling the caudal lung surface with it. Expiration is passive, with elastic recoil of the lungs returning them to their pre-inspiration position. During exercise or when ventilatory demand is increased, external intercostal, sternocleidomastoid, scalenus, and ventral serratus muscles are used to pull the ribs in a rostral direction and pull the lungs outward. Contraction of internal intercostal muscles and abdominal rectus muscles aids during expiration.⁹⁵

Air is moved in and out the alveoli following a pressure gradient. During inspiration, pressure in the alveoli is subatmospheric, which allows air to move in to the alveoli. Pressure at the end of inspiration is atmospheric; thus, airflow ceases. During expiration, positive alveolar pressure generated by elastic recoil moves air out of the lung.

During inspiration, ventilation has to overcome tissue elastance, alveolar surface tension, and airway resistance.¹⁰² Elastance is the degree to which the lung can return to its dimensions (recoil) after removal of the distending forces of inspiration. It is measured in unit volume change per unit of decreased pressure. Compliance is a measure of lung distensibility and is the reciprocal of elastance; it is measured as change in lung volume per unit pressure change. Pulmonary compliance can be estimated from pressure-volume loops obtained during the respiratory cycle and is equivalent to the slope of the pressure-volume curve (ΔV/ΔP) at any particular point. The steeper the slope of a pressure-volume curve, the greater the compliance. Normally, lung compliance is lowest at high and low lung volumes; thus, more energy is required to expand the lungs by the same volume at those points. Lung compliance can be modified by fibrosis or pulmonary edema.

Alveolar surface tension is generated at the air–liquid interface in the alveoli. Normally, it is low because of surfactant produced by alveolar type II cells. Surfactant indirectly increases lung compliance by lowering surface tension and reduces the amount of work needed to inflate the lungs. It also prevents collapse of small alveoli, and thus atelectasis, by permitting variation in surface tension with change in alveolar size. Airway resistance must also be overcome during inspiration and expiration. Contributors to inspiratory airway resistance during normal, quiet respiration include the nares (79% of total resistance during inspiration), larynx (6%), and small airways (15%).64,65,95 Expiratory resistance is 74% nasal, 3% laryngeal, and 23% small airways.

Alveolar ventilation is precisely controlled to match metabolic need; therefore, arterial oxygen pressure (PaO₂) and arterial carbon dioxide pressure (PaCO₂) vary minimally with physical activity. Ventilation is controlled by a respiratory center in the medulla that generates breathing rhythm and regulates tidal volume.99,102 Chemical and neural reflexes adjust ventilation to the needs of the patient, with chemoreceptor reflexes being the most important regulators. Changes in PaO₂, PaCO₂, and pH stimulate central and peripheral chemoreceptors, with the greatest response to changes in carbon dioxide. A small increase in PaCO₂ causes a substantial increase in ventilation, which returns PaCO₂ to original levels.

Response to changes in CO₂ is a result of stimulation of central chemoreceptors on the ventral surface of the medulla. Unlike HCO₃⁻ and H⁺, CO₂ can diffuse through the blood–brain barrier. When dissolved in the extracellular fluid, CO₂ is converted to HCO₃⁻ and H⁺, which stimulate the central receptors. Sensitivity to CO₂ is a result of two mechanisms: extracellular fluid has a lower pH than blood and less protein to buffer hydrogen ions, resulting in an increased sensitivity of central receptors to carbon dioxide variations. CO₂ also stimulates peripheral receptors in carotid and aortic bodies. The resulting ventilatory response is usually more rapid but of smaller magnitude than that seen with stimulation of central receptors.

Changes in PaO₂ have less effect on ventilation. If PaO₂ is below 60 mm Hg, however, ventilation increases, a reaction known as hypoxic ventilation drive. This reaction may be important for maintaining ventilation if CO₂ responsiveness has been altered by chronic lung disease or acid–base imbalance. Neural reflexes are also less important for control of normal ventilation. Stretch receptors in the airway and the lung parenchyma stop inspiration to prevent overinflation of the lungs, and upper airway reflexes protect the lung form foreign material by triggering bronchoconstriction and coughing when irritants are present.

A normal dog or cat moves approximately 10 mL of air per kg per inspiration to have adequate ventilation. A portion of that ventilation is alveolar, which is critical for gas exchange, and the remainder is dead space, which is important for other functions such as thermoregulation. Alveolar ventilation determines the amount of CO₂ in arterial blood: when PaCO₂ is increased, hypoventilation is present; conversely, when PaCO₂ is decreased, hyperventilation is present. Animals can change the ratio of dead space to alveolar ventilation by changing breathing patterns. Because panting dogs have a normal PaCO₂, they are not hyperventilating, even though total ventilation increases dramatically, because PaCO₂ is only altered by alveolar ventilation. Dead space itself can be significantly increased when alveoli are ventilated but not perfused (e.g., pulmonary thromboembolism).¹⁹

Gas Diffusion Across the Blood–Gas Interface

Diffusion of gas across the blood–gas interface follows Fick law, which states that rate of transfer of a gas through a sheet of tissue is proportional to surface area available for diffusion, diffusion coefficient of the gas, and difference in gas partial pressure between the two sides and inversely proportional to the tissue thickness (distance the gas must travel). At the blood–gas interface, the lungs have a surface area of 50 to 100 m² and a 0.3-µm thickness, which is ideal for diffusion. The diffusion coefficient of CO₂ is 20 times greater than that of oxygen; CO₂ therefore diffuses more rapidly.¹⁰⁰ Normally, this difference is inconsequential; however, oxygen delivery can become critical if the area for diffusion decreases and the diffusion distance increases, resulting in impaired delivery of oxygen (hypoxia) well before CO₂ removal is inadequate (hypercapnia).

Gas Transport by Blood

Oxygen and CO₂ are transported into the blood in different forms.¹⁰¹

Oxygen is transported in a dissolved state or in combination with hemoglobin (Hb). The amount of dissolved oxygen (0.003 mL O₂/100 mL of blood for each mm Hg of PO₂, or 3% per 100 mm Hg) is not sufficient to maintain adequate peripheral tissue oxygenation; therefore, most of the oxygen delivered to the peripheral tissue (98.5%) is bound to Hb. Hb is made of heme, an iron–porphyrin compound, joined to the protein globin, which consists of four polypeptide chains. Normal adult Hb is known as hemoglobin A, which can have ferrous and ferric forms. The ferric form is known as methemoglobin and is unable to carry oxygen.

Oxygen forms a reversible combination with Hb to produce oxyhemoglobin. The maximum amount of oxygen that can bind to Hb is called oxygen capacity, and the oxygen content is the actual amount of oxygen combined with Hb. Oxygen saturation, which is the fraction of Hb molecules in a blood sample that are saturated with oxygen at a given partial pressure of oxygen, is a ratio of oxygen content to oxygen-carrying capacity. One gram of pure Hb can combine with 1.39 mL of oxygen. Normal blood has about 15 gm of Hb/100 mL; therefore, the oxygen capacity is around 20.8 mL of oxygen/100 mL of blood. Oxygen saturation of arterial blood with a PaO₂ of 100 mm Hg is about 97.5%; saturation is 75% for venous blood with a PaO₂ of 40 mm Hg.

The oxygen–Hb dissociation curve describes the interaction between oxygen and heme. The curve has a very characteristic sigmoid form that represents several physiologic advantages (Figure 103-3). The flat upper portion means that a decrease in partial pressure in alveolar gas will have little effect on oxygen saturation when oxygen partial pressure is 80 mm Hg or more. Also, because oxygen diffuses along a positive-pressure gradient from the alveoli to capillary blood, oxygen reserve is large enough for sufficient oxygen to diffuse into the blood and saturate Hb. The steep part of the dissociation curve means that the peripheral tissues can withdraw a large amount of oxygen for only a small decrease in capillary oxygen partial pressure. The oxygen dissociation curve can be shifted to the right with acidosis and increased temperature, 2,3-diphosphoglycerate in red blood cells (RBCs), and CO₂ (Figure 103-4). It shifts in the opposite direction with the opposite causes. A rightward shift allows better unloading of oxygen, which is beneficial in peripheral tissue.

It is important to understand the relationship among Hb concentration, oxygen saturation, and partial pressure of oxygen, especially when working with a patient with anemia. Arterial oxygen content is given by the formula CaO₂ = (1.36 × Hb × %O₂Sat/100) + 0.003PaO₂. A patient with 15 g of Hb/dL, a PaO₂ of 100 mm Hg, and 97% oxygen saturation will transport 20.1 mL of O₂/100 mL of blood; a patient with 10 g of Hb/dL, PaO₂ of 100 mm Hg, and 97% oxygen saturation will only transport 13.5 mL of oxygen/100 mL of blood. This outlines the importance of early transfusion of patients with acute blood loss so as to improve oxygen-carrying capacity.

CO₂ is carried in the blood in its dissolved form (∼5% of transported arterial CO₂) and in chemical combination with proteins (primarily Hb) as carbamino compounds (∼20% of excreted CO₂); however, the majority is transported in the form of bicarbonate (Figure 103-5). Within RBCs, carbonic anhydrase accelerates transformation of CO₂ into carbonic acid, which dissociates into bicarbonate and hydrogen ions. Whereas bicarbonate ions diffuse along a concentration gradient back into plasma, hydrogen ions are trapped in RBCs. To maintain electrical neutrality and osmotic balance, respectively, chloride ions (Cl⁻) and water diffuse into the cells. The reaction continues to move to the right because Hb buffers the hydrogen ion. In the lungs, CO₂ is removed with ventilation, decreasing PCO₂ and reversing the effect.

Unlike oxygen, removal and uptake of CO₂ from the blood is almost directly related to PCO₂. Hb oxygen saturation has a major effect on CO₂ dissociation because deoxygenated Hb has a greater affinity for CO₂ than oxyhemoglobin. Deoxygenated (venous) blood therefore transports more CO₂ than oxygenated blood. The effect of changes in oxyhemoglobin saturation on CO₂ content in relation to PCO₂ is known as the Haldane effect.

Gas Exchange

Pulmonary gas exchange refers to the collective process by which O₂ and CO₂ are exchanged between the alveolus and the arterial blood.¹⁰³ Exchange of O₂ is complex and dependent on several factors, including diffusion across the alveolar–capillary membrane, amount of venous admixture in arterial blood, and relationship (or matching) of ventilation to perfusion. PaO₂ should be nearly equal to alveolar oxygen pressure (PAO₂) and should approach 100 mm Hg at sea level under normal physiologic conditions. Impaired gas exchange occurs when PaO₂ becomes less than PAO₂. The average alveolar partial pressure of oxygen can be calculated with the equation: PAO₂ = [FIO₂ × (Pbarometric − 47 mm Hg)] − [1.2 × PaCO₂], with FIO₂ = fraction of inspired oxygen (21% on room air) and PH₂O = 47 mm Hg. The alveolar–arterial oxygen difference can be calculated to quantify the severity of the gas exchange impairment using the formula: PA-aO₂ = PAO₂ – PaO₂ = [FIO₂ × (Pbaro − 47 mm Hg) − 1.2 × PaCO₂] − PaO₂. In a normal animal breathing room air, PA-aO₂ should be less than 10 mm Hg. If PA-aO₂ is greater than 30 mm Hg, there is severe gas exchange impairment.

Gas exchange impairment may be caused by diffusion impairment, ventilation-perfusion (V/Q) mismatch, or shunting. Diffusion impairment results from an increased thickness or decreased surface area of the alveolar membrane. Changes in the lungs have to be advanced to create diffusion impairment. Potential causes include chronic emphysema, pulmonary interstitial fibrosis, and early pulmonary edema. Shunt or venous admixture results from an anatomic shunt (e.g., right-to-left shunt in the heart). V/Q mismatch occurs when ventilation and perfusion are not closely matched in portions of the lungs. Whereas pulmonary thromboembolism results in an increase in V/Q, pneumonia or alveolar collapse (e.g., from pulmonary mass or pneumothorax) results in a decrease in V/Q. Response to oxygen should help differentiate between diffusion impairment, increased or decreased V/Q, and shunt. Animals with right-to-left shunting do not respond at all to oxygen, but patients with diffusion impairment respond extremely well and quickly. Whereas animals with increased V/Q have a good response to oxygen, animals with decreased V/Q have a very modest or poor response.

Consequences of Thoracotomy on Pulmonary Physiology

After thoracotomy, hypoxemia, residual pneumothorax, pleural effusion, and pain must be corrected to help restore normal pulmonary and cardiac physiology.⁹⁵

Intercostal Thoracotomy

Intercostal thoracotomy is employed when exposure to a specific region of the thoracic cavity is needed. This approach provides good access to thoracic structures in the immediate area of the thoracotomy; however, access to structures not in the area of the thoracotomy is limited. As a general rule, intercostal thoracotomy allows access to about one third of the ipsilateral thoracic cavity and mediastinal structures. Access to structures in the contralateral thorax is very limited when using this approach.

A lateral thoracic radiograph also can help determine the intercostal space that best exposes a desired thoracic structure. Because the hilus of the lungs is located between the fourth or fifth intercostal space, however, most intercostal thoracotomies for lung lobectomy are performed at one of those spaces. In general, cranial lung lobes are approached through the ipsilateral fourth or fifth intercostal space, caudal lung lobes through the ipsilateral fifth or sixth intercostal space, and right middle lung lobe through the right fifth intercostal space. A caudal intercostal thoracotomy may be combined with an incision in the diaphragm to provide exposure to the cranial abdominal cavity.

An intercostal thoracotomy starts with an incision through the skin and subcutaneous tissue with the cutaneous trunci muscle (see Figure 104-7). As a general landmark, the caudal-dorsal tip of the scapula lies at the level of the fourth intercostal space. The latissimus dorsi muscle is incised from ventral to dorsal with cautery to minimize intraoperative bleeding. After incising the latissimus dorsi muscle, intercostal spaces can be counted from cranial to caudal by palpating under the muscle and subcutis. After the appropriate intercostal space has been identified, the serratus ventralis muscle is separated between muscle fibers. Ventrally, the scalenus muscle is transected if the thoracotomy is cranial to the fifth rib and the rectus abdominis muscle is incised if caudal to the fifth rib. To spare the intercostal artery and nerve, intercostal muscles are incised close to the cranial border of the caudal rib in the intercostal space. Pleura is punctured to allow collapse of lung lobes and entry into the pleural space. The pleural incision is extended dorsally and ventrally as needed; ventrally, the internal thoracic artery should be identified by internal palpation along the sternum so as to avoid damage.

Before closing the thoracotomy, a thoracostomy drain is placed to establish negative pressure in the pleural space and monitor the pleural space in the postoperative period. To prevent air leakage in the postoperative period, the drain is tunneled underneath the latissimus dorsi muscle over two to three intercostal spaces.¹⁰⁷ The intercostal thoracotomy is closed by placing circumcostal sutures of 1-0 absorbable material to approximate the ribs. Alternatively, holes can be drilled in the caudal rib of the intercostal space to reduce the risk of intercostal nerve compression.⁷⁷ This technique has been associated with less postoperative pain; however, it can only be performed in large-breed dogs because of the risk of rib fracture.⁷⁷ Each muscle layer is closed with a simple continuous suture pattern with a 3-0 absorbable monofilament suture materials. The subcutaneous tissue and skin are also closed with continuous patterns.

Median Sternotomy

Median sternotomy is the only thoracic approach that allows access to the entire thoracic cavity and therefore is indicated when exploration of the thoracic cavity is necessary. For surgery of the lungs, this approach is preferred when pulmonary bullae or blebs are suspected. Structures in the dorsal thoracic cavity such as the great vessels and bronchial hilus are more difficult, but not impossible, to reach with a median sternotomy. Median sternotomy can be combined with a ventral midline celiotomy or cervical incision if a combined approach to the abdomen or neck is desired.

An important technical consideration when performing a sternotomy is that the manubrium, xiphoid, or both should be left intact. Doing so greatly enhances the ability to achieve a stable sternotomy closure, thereby decreasing the risk of postoperative complications. Reluctance to use this approach because of a perception that it is associated with excessive postoperative pain or complications is not justified. In dogs, pain, the degree of cardiopulmonary impairment, and complication rates with this approach are not different from those after intercostal thoracotomy.16,75,79 In humans, median sternotomy causes less postoperative discomfort than intercostal thoracotomy.^21,98 The decision to use a sternotomy or thoracotomy approach should therefore be based on the kind of access to the thoracic cavity needed, not on a perception that one approach is superior with regard to intraoperative or postoperative morbidity.

For a median sternotomy, the patient is placed in dorsal recumbency, and the skin is incised on midline from the manubrium to the xiphoid. The pectoralis muscle is dissected off the midline with electrocautery until the central line of the sternum is exposed (see Figures 104-10 to 104-14). Sternotomy is performed with a sternotomy or oscillating saw. If an oscillating saw is used, intrathoracic structures should be protected with a malleable retractor. The xiphoid or manubrium is left intact. A thoracostomy drain is placed before sternotomy closure, which is accomplished with cerclage wires in a figure of eight fashion around sternebrae to provide maximum stability.¹⁴ Stainless steel is preferred over nonabsorbable sutures, especially in large-breed dogs, because sutures are not strong enough to maintain apposition of the two halves of the sternum until it is healed.⁶⁹

Thoracoscopy

Thoracoscopy is a minimally invasive operative procedure for the examination of the pleural cavity and its organs. With the development of high-resolution microcameras, video optics, and fiberoptic light delivery systems, clear magnified images of the surgical field can be transferred to a video screen. The ability to perform diagnostic and advanced therapeutic procedures is possible with minimally invasive video-assisted endoscopy in combination with minimally invasive surgical instruments.

The basic equipment for thoracoscopy includes a surgical telescope, trocar-cannulas, a basic set of thoracoscopic surgical instruments, a light source, a video camera, and a video monitor. Thoracoscopy does not require CO₂ insufflation because the ribcage maintains the thoracic cavity in an expanded state. Telescopes used for thoracoscopy in small animals are most commonly 5 mm in diameter and forward-view 0-degree or forward oblique 30-degree telescopes. The 0-degree telescope allows a natural field of view and a normal perspective to organ orientation. The 30-degree telescope provides better visualization of parts of the thoracic cavity that are difficult to access; however, orientation and manipulation are more difficult with angled telescopes.

Numerous instruments are available for endoscopic exploration and surgery. The basic instrument set consists of grasping forceps, scissors, biopsy forceps, and a palpation probe. Forceps and scissors are isolated for electrocautery. Electrocautery can be used on small blood vessels during resection of mediastinum or pericardium. Pretied ligatures are available for lung biopsy; they eliminate the need for knot tying inside the thoracic cavity.

Thoracoscopy can be performed through a transdiaphragmatic or an intercostal approach. The intercostal approach is primarily used for surgical procedures such as partial or complete lung lobectomy. The transdiaphragmatic approach is preferred for exploration of the thoracic cavity and pleural space. For an intercostal approach, the patient is positioned in lateral recumbency. Cannulas are placed as needed within the fourth to ninth intercostal spaces. Cannulas should be inserted in the ventral two thirds of the intercostal space because the ribs are stiff along the most dorsal part of the intercostal space, making manipulation of instruments and camera difficult. The skin is incised to a size equivalent to cannula diameter. The thoracic wall is bluntly dissected with a mosquito forceps until the thoracic cavity is perforated. The cannula with its blunt trocar is introduced through the incision into the thoracic cavity. Three or four trocars are usually required to perform a thoracoscopy. Biopsy of hilar lymph nodes, sternal lymph nodes, lung lobes, or the pleural surface can be collected with this approach. Lung lobectomy is performed with an intercostal thoracotomy associated with one-lung ventilation.38,39

For the transdiaphragmatic subxiphoid approach, the patient is placed in dorsal recumbency. The first cannula is placed along the xiphoid underneath the last rib to access either the left or right hemithorax. The telescope is then introduced into the thoracic cavity for a preliminary evaluation. Two other cannulas are subsequently placed in the ninth or tenth intercostal space close to the sternum. After dissection of the mediastinum with electrocautery, both hemithoraces can be evaluated, and biopsies of the pleural surfaces, lung lobes, lymph node, or thymus can be collected. Partial lung lobectomy can be performed with this approach.

After completion of the thoracoscopy, a thoracostomy tube is placed in a routine fashion, and the cannulas are removed. The deep muscle layer is closed with a cruciate suture with 3-0 monofilament absorbable suture, and subcutaneous tissue and skin are closed in a routine fashion. If a transdiaphragmatic approach is used, the hole in the diaphragm is not repaired. The thoracic drain is maintained for 12 to 24 hours.

Congenital Diseases of the Lungs

Congenital disease of the lungs is either compatible or incompatible with life;⁴⁵ severe anomalies of agenesis or hypoplasia cause death shortly after birth. Hypoplasia of one lung or lung lobe is rarely diagnosed unless thoracic radiographs are taken or a necropsy is performed.⁸⁰ Congenital tracheoesophageal and bronchoesophageal fistulas are extremely rare in dogs and cats.^6,31,77

Cysts, Bullae, and Blebs

Cystic and bullous lesions in the lungs are characterized by a thin-walled cavity within the lung parenchyma.2,45,60 Cysts can be fluid filled or air filled and are covered by a respiratory epithelium.^4,60 Blunt trauma to the chest with pulmonary contusion seems to be the most common cause of pulmonary cysts in dogs and cats, and younger animals appear to be at greater risk.⁴ An infected cyst will become a pneumatocele or an abscess, with destruction of respiratory epithelium. Pneumatocele can also result from pneumonia.⁶⁰

Lung bullae and blebs (pseudocysts) are similar to cysts; however, they have no epithelial lining.7,34,35,60 Bullae and blebs are described as large blisters with fibrous walls. Bullae are large air spaces that develop within the lung parenchyma, and blebs are small accumulations of air between the parenchyma and visceral pleura (Figure 103-6).² These cavities develop from traumatic rupture and coalescence of alveoli and are frequently secondary to obstructive lung disease.^{34,35,42,45,60} Pulmonary bullae have been reported in 16% of dogs with pulmonary blastomycosis, most often in association with an alveolar pattern.¹²

Bullae and cysts show similar complications of infection: abscessation; rupture, resulting in pneumothorax; and local compression of lung tissue, leading to dyspnea, exercise intolerance, and abdominal respiration.⁶⁰ Auscultation may reveal decreased ventilation sounds on the affected side and increased heart sounds on the contralateral side (displaced heart from a space-occupying cyst).

Spontaneous idiopathic pneumothorax warrants close examination of radiographs detailing lung profile and parenchyma for bleb, bullae, or cyst formation.42,72 Radiographs usually reveal unilateral or bilateral pneumothorax and occasionally pneumomediastinum; unfortunately, however, bullae or blebs are usually not identified.⁴² Computed tomography (CT) has been recommended for the diagnosis of bullae in dogs with spontaneous pneumothorax.^5,30,41 Atelectasis of the lobe containing the ruptured cavity may obscure underlying cysts.

Conservative management of spontaneous pneumothorax by continuous intrathoracic drainage can be attempted for 2 to 3 days before partial or complete lobectomy is considered.27,42,72 Many patients improve with conservative therapy, but recurrence rate is high.⁷² In a study of 12 dogs, none responded to conservative treatment with thoracocentesis or thoracostomy tube placement. Lung lobectomy is the treatment of choice for spontaneous pneumothorax in dogs.⁴² The preferred approach is a median sternotomy because dogs commonly have more than one lesion, and many lesions are bilateral.⁴² Most dogs have lesions in the cranial lung lobes, but other lobes can be affected concurrently. If the bulla or bleb cannot be visualized, the thorax is filled with warm saline so that leaks can be identified during ventilation. Visible lesions are removed by partial or complete lung lobectomy, often with a stapler. Resected tissues should be submitted for culture and histologic evaluation if underlying conditions are suspected. In one study, recurrence was not reported in 12 of 12 dogs after partial or complete lobectomies for bullae and blebs.⁴²

Thoracoscopy has been used to evaluate visceral surfaces for additional cysts and locating the ruptured cavity;⁸ however, thorough evaluation of the entire lung surface can be difficult with this modality. Mechanical pleurodesis can be attempted at the time of surgery to induce complete pleural adhesion and reduce the risk of recurrence; unfortunately, successful production of a complete adhesion for control of the disease is uncommon in dogs.²⁹