Entrance of air into the pleural space causes intrapleural pressure to become positive, which results in collapse of the lungs with a subsequent drop in venous return and cardiac output. Pneumothorax can be closed or open depending on whether or not there is communication between the pleural space and outside the thorax. The most common causes of pneumothorax in dogs are likely blunt force trauma from car collisions or penetrating trauma from an inhaled foreign body. Exposure to porcupine quills has also resulted in pneumothorax in the northern United States and Canada (Sevy et al. 2023). In the cat, blunt trauma occurs from a car accident or fall from a height, although inflammatory lower airway disease is also a common cause of pneumothorax (Mooney et al. 2012). In dogs or cats, esophageal perforation can lead to pneumothorax, and it can also result from rupture of an emphysematous bulla, pleural bleb, neoplasm, Paragonimus cyst, or abscessed lung lobe. Lung necrosis due to embolization associated with heartworm disease or pulmonary thromboembolic disease has also been implicated in pneumothorax. Barotrauma during anesthesia or mechanical ventilation is recognized as an iatrogenic cause of pneumothorax and it can also occur post‐thoracocentesis or fine‐needle lung aspiration. Multiple lung lobes can be involved depending on the underlying disease process, and cranial lobes are affected most commonly in spontaneous pneumothorax. A specific form of pneumothorax is a tension pneumothorax, where a piece of pulmonary tissue or pleura acts as a ball valve, allowing passage of air into the pleural space during inspiration, with obstruction of escape of air via the same pathway. In this situation, air continues to accumulate in the pleural space, leading to a continual rise in intrapleural pressure and circulatory collapse. Tension pneumothorax is sometimes encountered in animals with pleural fibrosis secondary to a long‐standing exudative effusion that develop a rent in the pleura allowing air to escape into the pleural cavity. Immediate thoracocentesis is required to allow lung expansion and to restore cardiac output. Any age or breed of dog or cat can develop pneumothorax depending on the underlying etiology. An animal kept out of doors is at increased risk for traumatic injury or foreign body inhalation, while a hospitalized patient would be more likely to develop iatrogenic injury. Spontaneous pneumothorax associated with underlying lung disease appears to be more common in young to middle‐aged deep‐chested dogs. The primary clinical complaint associated with pneumothorax is difficulty breathing or tachypnea that develops immediately after an injury or rupture of a pulmonary lesion. Signs can be acute in onset, however with foreign body inhalation or quill exposure, they can occur 2–6 months after the episode (Gibson et al. 2019; Sevy et al. 2023) Some cases with spontaneous pneumothorax lack a history of signs referable to the respiratory tract and will display chronic, non‐specific signs of lethargy and anorexia, prior to the development of acute, worsening respiratory difficulty associated with accumulation of air in the pleural space. Accumulation of air in the pleural space untethers chest expansion to lung expansion, leading to rapid and shallow breathing and dampening of lung sounds. Air in the pleural space will rise, leading to an absence of breath sounds dorsally and hyperresonance on percussion. Lung sounds might be heard in the ventral lung fields only. Animals involved in traumatic encounters should be closely evaluated for additional injuries, including broken ribs, lung damage, and cardiac bruising. Pulmonary contusions coincident with pneumothorax can lead to harsh lung sounds focally and myocardial contusions can result in tachycardia or an arrhythmia. In some cases of foreign body inhalation, a grass awn can form a palpable abscess on the body wall or can be seen migrating out of the subcutaneous space. Pneumothorax is usually bilateral because the mediastinum is incomplete. It is recognized radiographically by an absence of lung parenchyma and pulmonary vasculature in the periphery of the lung. The heart is typically lifted off the sternum on the lateral view (Figure 7.1). Pneumothorax can also be detected on thoracic ultrasound by an absence of the “glide sign,” which is the movement of normal lung along the pleura. While pneumothorax is readily apparent on thoracic radiographs, the underlying lesion is often not visible, particularly when bullous lung disease or pleural blebs are the cause of the pneumothorax. Cross‐sectional imaging with computed tomography (CT) improves definition of lung regions (Figure 7.2); however, it has low sensitivity for detection of bullae associated with spontaneous pneumothorax (Reetz et al. 2013). Figure 7.1 (a) Right lateral and (b) dorsoventral radiographs from a 7‐year‐old spayed female (FS) Australian Shepherd with recurrent episodes of spontaneous pneumothorax demonstrate collapse of the right cranial lung lobe. Figure 7.2 Computed tomographic slice through the caudal thorax of a 6‐year‐old male intact (MI) Labrador Retriever with spontaneous pneumothorax. A soft tissue structure is present in the distal portion of the right caudal lung lobe. Histopathology revealed a pulmonary adenocarcinoma. For animals with suspected exposure to Paragonimus, a trematode that employs snails and crustaceans as intermediate hosts, a fecal sedimentation or zinc sulfate centrifugation–flotation should be performed. Paragonimus kellicotti is endemic in Canada and in the USA (typically the Midwest or Gulf states), while in Japan, boar‐hunting dogs are at risk for infection by Paragonimus westermani (Kirino et al. 2008). Paragonimiasis is recognized as a shared zoonosis (affecting both animals and humans) and is caused by ingestion of the crayfish intermediate host, which migrates from the peritoneal cavity through the diaphragm to enter the lungs. The trematode has not yet been reported in Europe. In infected dogs, thoracic radiographs or CT can show multiple thin‐walled cavitated cysts, while in cats, thick‐walled granulomatous lesions and pleural involvement are more typical. Thoracocentesis should be performed when pneumothorax is suspected and it might be required as a life‐saving procedure prior to radiographic or ultrasonographic confirmation of air accumulation. With traumatic pneumothorax, a single chest tap with alleviation of respiratory difficulty through sedation and administration of oxygen will often restore pleural integrity and result in cure. If Paragonimus is diagnosed, praziquantel (25 mg/kg orally [PO] three times a day [TID] for 3 days) or fenbendazole (50 mg/kg/day for 2 weeks) can be employed to treat infection (Bowman et al. 1991), although surgical resection of the diseased lung regions can be required. If air continues to accumulate within the pleural space after several chest taps, placement of a chest tube should be considered (see Chapter 3). Generally, spontaneous pneumothorax and tension pneumothorax will require placement of a chest tube and constant thoracic drainage to resolve air leakage. Because underlying lung disease is often present with spontaneous pneumothorax, surgical intervention is usually required to avoid recurrence. Therefore, when pneumothorax does not resolve within 3–5 days or if parenchymal lesions causing pneumothorax are visualized on radiographs, an exploratory thoracotomy should be performed. Pre‐operative CT is usually performed to investigate possible pulmonary lesions. Video‐assisted thoracoscopy is a minimally invasive procedure that can be used to investigate and manage causes of pneumothorax; however, it has a high rate of transition to an open approach in cases with bullous disease (Case et al. 2015). In that event, median sternotomy is usually preferred to allow full exploration of the lungs. When thoracotomy is not possible, use of autologous blood as a pleural patch can be considered. To perform this, the dog or cat is sedated or anesthetized, a sterile preparation of the thoracic wall is performed, and the chest is evacuated of air. Fresh whole blood (5–10 ml/kg) is collected aseptically from the jugular vein and injected immediately into the pleural space through a chest tube or catheter to achieve pleurodesis. Isotonic fluids are administered intravenously to replace the blood withdrawn. In one study, pneumothorax resolved after one treatment in four out of eight dogs (Oppenheimer et al. 2014). Traumatic pneumothorax generally has a good prognosis if myocarditis and pulmonary contusions do not complicate the presentation. The prognosis for spontaneous pneumothorax depends on the underlying disease responsible for air leakage. Surgical resection of the affected area is associated with an excellent outcome in most dogs with emphysematous lung disease, foreign body pleuropneumonia, or Paragonimus infection; however, the presence of neoplasia can warrant a guarded prognosis, depending on the extent and type of the neoplasm. The mediastinum is a potential space running through the middle of the thorax from the thoracic inlet to the diaphragm and the sternum to the vertebral column (Figure 7.3). It is continuous with the fascial planes in the neck and retroperitoneal space and contains the carotid arteries, vagosympathetic trunks, trachea, esophagus, and cranial vena cava cranially, the heart and great vessels in the mid‐section, and the esophagus caudally. It is lined by pleura and excludes the left and right lung. Pneumomediastinum is an accumulation of air around the structures in the cranial mediastinum. It occurs most commonly from endotracheal tube injury or over‐inflation of the cuff, traumatic jugular venipuncture, or a transtracheal wash. It can also result from trauma associated with a dog fight, from over‐ventilation during anesthesia, or due to bronchial injury from a foreign body or neoplastic infiltration. Emesis is a cause of pneumomediastinum in the cat. A leaky tracheostomy tube can result in pneumomediastinum. Finally, pneumomediastinum can occur with bronchial, tracheal, or alveolar rupture when air tracks along fascial planes to reach the mediastinum. Spontaneous or idiopathic pneumomediastinum has been reported in approximately one‐third of cases in cats (Thomas and Syring 2017) and an unknown number of dogs. Pneumothorax can be found in conjunction with pneumomediastinum, particularly when the cause is traumatic. Figure 7.3 Thoracic radiographs with red markings outlining the boundaries of the mediastinum. Any age of dog or cat can be affected. Usually a history of trauma or iatrogenic injury is present immediately prior to the onset of signs or within a week of presentation. In cats, a recent dental procedure is often found in the history, with tracheal rupture resulting from damage to the dorsal tracheal membrane at the thoracic inlet. Respiratory difficulty can be noted or owners might detect subcutaneous emphysema concentrated over the neck, thorax, and head. Frequently clinical signs are absent, and pneumomediastinum is an incidental finding on radiographs following a venipuncture or tracheal wash. Pneumomediastinum often does not result in any respiratory abnormalities but coincident subcutaneous (SQ) emphysema can be detected as a crackling under the skin during palpation. In some cases, this SQ emphysema can restrict ventilation. In more severely affected animals, tachypnea and respiratory distress can occur, or collapse can result from pneumomediastinum accompanied by pneumothorax. When pneumothorax is present, lung sounds are absent dorsally. Diagnosis is based on radiography. Pneumomediastinum is evident when outer borders of the trachea, esophagus, carotid arteries, aorta, and azygous veins are visible because of contrast with mediastinal air. Subcutaneous emphysema is often detected over the trunk (Figure 7.4). If tracheal rupture is suspected, tracheoscopy can occasionally be helpful in locating the lesion. Surgical exploration is usually required when conservative measures fail. Generally no specific treatment is required for pneumomediastinum and air will resorb within 10–20 days. Air resorption is hastened by placing the patient in an oxygen‐enriched environment. This will decrease the work of breathing to facilitate sealing of any rents in the tissue and hasten oxygen resorption by creating a more favorable oxygen gradient for diffusion. Judicious use of sedatives to reduce stress is important. In rare instances when subcutaneous emphysema is severe and causes restriction of ventilation, needle aspiration of air trapped under the skin can sometimes be helpful. Concurrent pneumothorax requires thoracocentesis. If tachypnea or respiratory effort increases, surgical repair of the lesion is necessary. Figure 7.4 Right lateral radiograph from an 18‐month‐old spayed female domestic short hair (FS DSH) that had been anesthetized 2 weeks previously and developed pneumomediastinum and subcutaneous emphysema. Prognosis is usually excellent for resolution of disease. When pneumomediastinum is detected, restraint methods and diagnostic techniques should be reviewed for predisposing features that might have led to airway injury. In cats undergoing anesthesia, <3 ml of air is required for sufficient inflation of the endotracheal tube cuff. Blunt trauma to the abdomen from a car accident or fall from a height increases intracavitary pressure, leading to rupture of the muscular portion of the diaphragm and herniation of abdominal organs into the thoracic cavity. The liver is involved most frequently, followed by the small intestine and stomach. The lungs collapse because of loss of contact between visceral and parietal pleura that would normally coordinate thoracic excursions to lung expansion. Compression by abdominal organs also contributes to lung collapse. Fluid accumulation in the thorax due to hemorrhage or transudation from the organ surface further restricts lung expansion and worsens oxygenation and ventilation. Animals with herniation of the stomach into the chest cavity can suffer rapid decompensation if aerophagia results in continual expansion of the stomach. The space‐occupying effect of gastric dilation augments lung compression, with a decrease in venous return and subsequently cardiac output. Congenital diaphragmatic hernias that can affect dogs or cats include pleuroperitoneal or peritoneopericardial diaphragmatic hernias (PPDH). Of these, PPDH is more common. It is likely related to trauma or a failure of development during the embryonic stage of growth. In some cases, other congenital lesions such as umbilical hernia, pectus excavatum, or congenital heart defects can be recognized concurrently (Burns et al. 2013). Affected animals can have an acute history of trauma within the past several hours or may have experienced injury weeks to years in the past. Most dogs and cats are young (3–4 years) because these are the individuals that are more often exposed to traumatic events, and those with congenital hernias can be very young at the time of diagnosis. PPDH is more common in cats than in dogs (Burns et al. 2013). Clinical signs are usually respiratory in origin and include tachypnea and difficulty breathing, but some animals are presented for acute or chronic vomiting or regurgitation associated with gastrointestinal (GI) obstruction or strangulation. Still others can develop progressive exercise intolerance or respiratory difficulty associated with gradual accumulation of pleural fluid from organ transudation. With PPDH, extrusion of abdominal organs into the pericardial sac can result in GI signs or signs of cardiac tamponade, including ascites or collapse. In some animals, PPDH is an incidental finding. Animals with organ herniation or pleural effusion often have muffled heart and lung sounds ventrally or on one side of the chest. When intestinal herniation has been present for >24–48 hours, borborygmi can sometimes be auscultated over the thorax (Figure 7.5). Occasionally, abdominal palpation will reveal an absence of contents. Traumatic injury to other structures in the thorax, abdomen, or skeleton can be found in 25–40% of cases, and a complete physical examination should be performed to detect findings consistent with traumatic myocarditis, urinary system rupture, rib fractures, or orthopedic injuries (Gibson et al. 2005). Thoracic and abdominal radiographs can usually confirm the diagnosis of a diaphragmatic hernia; however, if pleural effusion is present, thoracocentesis and repeat radiographs might be required to provide definition of the diaphragmatic silhouette and thoracic structures. Chronic cases are often more difficult to diagnose radiographically. A barium series can confirm the presence of intestines in the thoracic cavity or better define the position of the liver or small intestines, and ultrasound can occasionally be helpful. However, CT and/or exploratory surgery can be required for confirmation of the diagnosis. With PPDH, the most remarkable finding on thoracic radiographs is massive cardiomegaly and loss of distinction of the border of the diaphragm. Echocardiography is useful for confirming the presence of organs in the pericardial space as well as investigating possible concurrent congenital cardiac disease. However, echocardiography can be challenging to perform because of constriction of structures by the pericardial sac. Figure 7.5 (a) Right lateral and (b) dorsoventral radiographs of a 2‐year‐old cat presented for chronic increased respiratory effort and periodic wheezing. Heart and lung sounds were muffled bilaterally. Herniation of the small intestine and proximal colon into the pleural space is noted. Surgical repair of the diaphragm is indicated for traumatic diaphragmatic hernia and is usually performed in animals with clinical signs associated with PPDH. Animals with chronic diaphragmatic hernias and those that are subclinical for PPDH do not necessarily require surgery. Standard stabilization methods with intravenous fluid support and withdrawal of pleural fluid prior to anesthesia are important, although cases with stomach herniation generally represent a surgical emergency because respiratory difficulty causes aerophagia, progressive stomach distention, and further cardiorespiratory compromise. When surgery is pursued, artificial ventilation must be provided to create lung expansion once the abdominal cavity has been opened. Oxygenation, ventilation, and cardiac rhythm must be monitored carefully throughout the procedure. Improvements in anesthetic drugs, monitoring, and assisted ventilation have vastly improved response to surgery. Diaphragmatic hernia repair is associated with an 80–90% survival rate (Gibson et al. 2005; Burns et al. 2013), regardless of whether the hernia is acute or chronic in nature and regardless of the time between admission and surgery. Owners should be aware that additional surgery might be required to repair soft tissue or orthopedic injuries that are not as life‐threatening as the diaphragmatic hernia. In cats with chronic diaphragmatic hernia, there is concern about development of re‐expansion pulmonary edema when abdominal contents are removed from the thoracic cavity. Controlled expansion of the lungs during the procedure might diminish occurrence of this, but typically re‐expansion injury carries a grave prognosis because it is not responsive to supportive therapy. Older animals with PPDH diagnosed as an incidental finding can have extended survival and excellent quality of life without surgical intervention. The etiology of pyothorax cannot always be determined. Bacteria can enter the pleural space through a bite wound, penetrating injury, foreign body inhalation, direct puncture of the chest wall, or esophageal rupture. Less commonly, bacteria can spread to the pleura from a pulmonary infection or hematogenously. In dogs, foreign body inhalation is often believed to be the most common etiology, while in cats, bite wounds are suspected, despite the fact that external evidence of wounds is often lacking (Johnson et al. 2023). Iatrogenic pyothorax results when aseptic technique is breached during thoracocentesis. Infection can be involve a single species of bacterium (Eiras‐Diaz et al. 2021; Kramer et al. 2021) but is often multi‐microbial (Walker et al. 2000; Johnson et al. 2023), and the anaerobic environment within the pleural space promotes growth of various types of bacteria. A rare cause of pyothorax in cats in some areas of the world is infection with the organism Rhodococcus equi (previously Corynebacterium equi or Mycobacterium equi). This organism is well known to cause pulmonary infection in foals and has rarely been documented to cause infection in cats in the US, Italy, and Australia, with more cases reported in Malaysia (Aslam et al. 2020). Disease is caused by inhalation or ingestion of a Gram‐positive coccobacillus found in manure, and interestingly, exposure to horses was not common for cases encountered in Malaysia. Outdoor cats <1 year of age were most commonly affected and exhibited a neutrophilic leukocytosis with monocytosis and thrombocytopenia. Some cats had skin lesions rather than pleural infection, and mortality was high (58%) despite some positive responses to marbofloxacin or azithromycin combined with rifampin (Aslam et al. 2020). Pyothorax most commonly occurs in young, outdoor animals. Large breed or hunting dogs and cats from multi‐cat households are affected most often. In some animals, clinical signs are primarily respiratory in origin, with tachypnea or labored breathing; however, however, more animals have prominent systemic signs, including weight loss, anorexia, inactivity, and exercise intolerance. Clinical signs can be present for days to months before presentation. Pyothorax is anticipated to result in a rapid, shallow breathing pattern; however, both the rate and amount of fluid accumulation influence the severity of respiratory difficulty, and respiratory rate can be only mildly elevated in some cases. Fever may or may not be present at the time of presentation, despite the presence of severe infection. Muffled heart and lung sounds are expected ventrally, although pyothorax can affect a single side of the thorax when the proteinaceous fluid occludes fenestrae in the mediastinum to create non‐communicating halves to the thorax. This could result in unilateral absence of lung sounds and could potentially displace cardiac sounds. Careful physical inspection of the thoracic wall will occasionally reveal recent or healed bite wounds or areas where foreign material has migrated out of the thoracic cavity. In chronically affected animals, hematology usually shows a mild normocytic, normochromic, non‐regenerative anemia in conjunction with leukocytosis characterized by neutrophilia and monocytosis. Increased serum globulin is a non‐specific indicator of chronicity and a marked inflammatory response, and this can result in a compensatory drop in serum albumin. Thoracic radiographs reveal unilateral or bilateral pleural effusion with obscuring of the cardiac silhouette and diaphragm, scalloping of ventral lung margins, and blunting of costophrenic angles (Figure 7.6). Evidence of a foreign body or a consolidated lung lobe is occasionally present. Thoracic ultrasound can be helpful in revealing flocculent or viscous pleural fluid and can sometimes detect lobar consolidation or the linear appearance of a foreign body. Figure 7.6 (a) Right lateral and (b) ventrodorsal radiographs from a 6‐year‐old castrated male (MC) Labrador Retriever presented for a 2 week history of anorexia and weight loss. Physical examination revealed absent lung sounds ventrally, and radiographs confirmed the presence of pleural fluid obscuring the cardiac silhouette and blunting of the costophrenic angle, particularly on the right side. The initial step in confirming a diagnosis of pyothorax is to perform thoracocentesis (see Chapter 2). Cytologic analysis reveals an exudative fluid (high protein and high cell count) comprised primarily of degenerate neutrophils. Intracellular bacteria (Figure 7.7) are observed in 62–93% of cats and 68–73% of dogs (Walker et al. 2000; Kramer et al. 2021; Johnson et al. 2023) despite previous antibiotic therapy. Both aerobic and anaerobic cultures should be requested on a pleural exudate because mixed bacteria are usually found (Table 7.1). Note that special transport medium is sometimes required to obtain an accurate result for anaerobic bacteria. A point of care test that assesses luminescence released by bacterial ATP (Test&Treat Ltd., Kentford, Newmarket, UK) shows promise in assisting in the diagnosis of a septic effusion (Vezzi et al. 2024). Similar to cytology, previous antimicrobial therapy does not appear to impact the result, although large‐scale studies are lacking. Hemorrhagic effusions cannot be accurately assessed and a 30 minute incubation period is required; however when cytologic assessment is not immediately available, a positive test could aid in the early diagnosis of pyothorax. Figure 7.7 Pleural fluid cytology from a cat with pleural effusion reveals degenerate neutrophils and intracellular bacteria (arrows) consistent with pyothorax. Table 7.1 Organisms commonly identified in animals with pyothorax. Successful treatment of pyothorax usually requires placement of uni‐ or bilateral chest tubes (see Chapter 3). The use of thoracic lavage with warm saline (10–20 ml/kg 2–4 times a day [BID–QID]) is controversial, but it can be helpful in reducing the amount of inflammation present in the pleural space. Addition of heparin to the lavage fluid (1500 units/100 ml) is also controversial, although some clinicians believe it can reduce adhesions and promote drainage. When lavage is used, the fluid is left in the chest cavity for <1 hour and then aspirated. The patient resorbs 10–25% of the fluid and it is not possible to retrieve all fluid, therefore some will be left in the pleural cavity. There is no advantage to adding antibiotics to the lavage fluid because the primary route of exposure of the pleura to antibiotics is through the systemic circulation. Intravenous fluids are typically used for supportive care as needed, and this also allows systemic administration of broad‐spectrum antibiotics that are active against both aerobes and anaerobes. Anaerobic coverage should be provided even if cultures are negative due to the difficulty in isolating anaerobic bacteria in some instances. Penicillins, cephalosporins, and clindamycin can be used in combination with a fluoroquinolone. Trimethoprim‐sulfa is often employed if infection with Nocardia spp. is suspected, although long‐term therapy contains the risk of side effects, including keratoconjunctivitis sicca, thrombocytopenia, hypothyroidism, anemia, and fatal liver toxicity. Each day before instituting thoracic lavage, fluid is extracted from the pleural cavity to evaluate the number and type of cells present and to check for the presence or absence of bacteria. Successful therapy is indicated by a reduction in cell numbers and decline in intracellular bacteria over several days of treatment. Medical therapy can take 3–7 days to be effective. Thoracic radiographs, ultrasound, or CT are used as indicated to detect a mass lesion or foreign body. Prior to removal of the chest tube, a fluid sample should be submitted for aerobic and anaerobic culture to ensure successful resolution of infection. Thoracotomy or video‐assisted thoracoscopy is required to remove a foreign body or to debride necrotic lung or mediastinal tissue. Surgical exploration is indicated when new radiographic findings are detected or if cell numbers or bacteria rise despite lavage and drainage therapy. Preoperative CT can help localize disease. In areas where foxtails are prevalent, bronchoscopy is often performed prior to surgery to remove foreign material and potentially salvage a lung lobe affected by foreign body pneumonia. For owners lacking sufficient funds for intensive hospitalization and treatment, consideration can be given to conservative medical management. One study reported successful management of 15 dogs with pyothorax by use of a single pleural drainage and antibiotics (ampicillin TID with metronidazole BID most commonly) for >6 weeks (Johnson and Martin 2007). The risk of persistent or recurrent infection must be communicated to the client if this mode of therapy is chosen. Short‐term survival in animals with pyothorax ranges from 72% in cats (Kramer et al. 2021) to 85% in dogs (Eiras‐Diaz et al. 2021), however the debate regarding the benefits of medical versus surgical treatment of pyothorax is difficult to resolve because surgery is often delayed until medical therapy has failed or is undertaken because an obvious need for surgical intervention is noted, such as a foreign body or mass lesion. Dogs might be taken to surgery earlier in the course of disease because of the increased likelihood of a foreign body as the cause of pyothorax. Overall survival rates beyond 70% can be anticipated when aggressive medical and surgical treatment is pursued. Lack of surgical debridement or early discontinuation of antibiotics can allow recurrent infection, and chronic pyothorax can be associated with fibrosing pleuritis (see section on chylothorax). Mediastinitis is an infectious or inflammatory process involving the cranial or caudal mediastinum. It can be caused by bacteria directly inoculated into the mediastinum through the thoracic wall or entering via an esophageal or tracheal route. Because the accessory lung lobe is commonly involved in foreign body inhalation, migration through the airway into the caudal mediastinum can result in a contained abscess (Figure 7.8). A cranial mediastinal mass effect can result from fungal infection causing enlargement of mediastinal lymph nodes (see Chapter 6) or by neoplasia (thymoma or lymphoma most commonly). Finally, mediastinal hemorrhage from rodenticide intoxication can result in a similar clinical picture to an infectious or inflammatory etiology. It is important to consider ingestion not only of the rodenticide, but also of the animal killed by the poison. Figure 7.8 (a) Lateral scout image from computed tomography and (b) a cross‐sectional image demonstrate a fluid meniscus through a caudal mediastinal abscess in the region of the accessory lung lobe. The red line in (a) approximates the level of the cross‐sectional image. Spirocerca lupi, a worm that lives in the esophagus or stomach of the dog and causes neoplastic transformation of tissue, can cause caudal mediastinitis. Spirocerca has a world‐wide distribution, but is found more often in warm climates, and disease appears to occur most commonly in Israel. A dog becomes infected with Spirocerca by eating a coprophagous beetle intermediate host or an animal that has eaten the beetle. The larvae gain access to the circulation and travel to the aorta, where they enter the esophagus. Adult worms (5–7 cm in length) live inside nodules in the esophagus, and rupture of the nodule can result in mediastinitis. Usually infection either is subclinical or results in neoplastic transformation of tissue. Young, outdoor dogs are more likely to develop fungal infection as well as gain exposure to foreign bodies, rodenticides, or dead animals through foraging behavior. Outdoor dogs and dogs that hunt are also more likely to be exposed to injury or foreign bodies and also to the carriers of a disease such as Spirocerca. Animals with mediastinitis can present with non‐specific complaints of anorexia, weight loss, and lethargy, more localizing signs related to respiratory compromise caused by obstructed breathing, or signs due to esophageal impingement can be noted. Esophageal disease related to injury or spirocercosis generally results in signs of difficulty swallowing or regurgitation. Esophageal rupture is associated with acute onset of pain, labored respirations, and tachypnea. The respiratory pattern is altered depending on the type and location of infection and any subsequent mass effect. Large mass lesions compress the trachea and result in inspiratory obstruction and stridor. In some cases, expiration can also be compromised and loud wheezing noises are heard. If pleural effusion develops secondary to a mass effect, tachypnea would be expected. Due to the proximity of neurovascular bundles to the mediastinum, a cranial mediastinal mass effect can disrupt venous return, resulting in edema of the front limbs, neck, and face (cranial vena caval syndrome), and interruption of nerve transmission. Neurological signs are primarily manifest as Horner’s syndrome (ptosis, enophthalmos, protrusion of the third eyelid, and miosis; Figure 7.9) and laryngeal paresis or paralysis might be recognized by inspiratory effort with stridor. Figure 7.9 This 9‐year‐old spayed female (FS) Mix breed dog demonstrates ptosis, enophthalmos, protrusion of the third eyelid, and miosis of the left eye consistent with Horner’s syndrome on the left. Fever is expected with systemic fungal infections and with bacterial infection in the mediastinum. Depending on the level of lung or pleural involvement, abnormal lung sounds can be auscultated, with muffling of lung sounds ventrally detected most commonly. A mass lesion or hemorrhage that affects primarily one side of the mediastinum can cause a shift in heart sounds away from the lesion and loss of lung sounds in the affected area. In cats and small dogs with mediastinitis, it can sometimes be difficult to compress the cranial thorax. The mediastinum is not usually visualized on thoracic imaging in normal animals except in brachycephalic dogs, which typically have a widened cranial mediastinum (Figure 7.10). If history, physical examination, or routine blood work suggest that a coagulopathy could be playing a role in the clinical presentation, prothrombin time (PT)/partial thromboplastin time (PTT) should be performed prior to invasive testing that could worsen bleeding (see Chapter 2). In diseased animals, radiographs can reveal a mass effect within the cranial or caudal mediastinum. Delineation of a lesion can require contrast esophagoscopy or angiography, although CT is often employed instead to outline the lesion more precisely. Ultrasound of cranial mediastinal masses is useful to determine whether the mass lesion is cystic or solid and to determine vascularity. Cytology of an aspirate can confirm neoplasia, as well as fungal or bacterial infection, which will help determine the need for medical versus surgical therapy. Aerobic and anaerobic culture of aspirated material is recommended when bacterial infection is suspected, because Bacteroides spp. are often involved in the disease process. Figure 7.10 Dorsoventral radiograph from a Bulldog demonstrates widening of the cranial mediastinum. Spirocercosis most typically results in a caudal mediastinal mass; aortic mineralization or spondylitis in the caudal thorax can also be detected (Dvir et al. 2001). Diagnosis is confirmed by finding small, elongated nematode eggs in a fecal flotation, or by documenting nodular lesions within the esophagus using radiography or endoscopy. Bacterial mediastinitis represents an encapsulated abscess. Surgical drainage in combination with the use of antibiotics with a good spectrum against oral and GI flora are indicated. Antifungal medication will generally resolve lymphadenopathy associated with fungal infection. Coagulopathic conditions resulting in mediastinal hemorrhage are treated with vitamin K1 (see hemothorax). Spirocerca can be eliminated with various anthelminthics, including fenbendazole and albendazole, although long‐term therapy with ivermectin or milbemycin oxime may be needed. Ivermectin should not be used in Collie‐type dogs. If surgery is required to repair the esophagus or to remove a large helminth granuloma, prognosis is guarded for recovery. Development of neoplasia secondary to spirocercosis is a recognized complication that can result in death due to primary or metastatic disease. The most common mass lesions in the cranioventral mediastinum are thymoma and lymphosarcoma. Thymoma is a unique neoplasm that can trigger auto‐immune paraneoplastic syndromes, with myasthenia gravis being one of the more common events (Robat et al. 2013; Hague et al. 2015). Mediastinal lymphoma has been associated with feline leukemia virus positivity to a variable extent depending on geographic location and overall FeLV positivity. Heart base tumors (chemodectomas), ectopic thyroid neoplasia, or metastatic lymphadenopathy can be found craniodorsally or in the perihilar region (Figure 7.11). Neoplastic mass lesions must always be distinguished from a granuloma or an abscess. Figure 7.11 Right lateral radiograph from an 11‐year‐old Labrador reveals a mass lesion at the heart base consistent with a chemodectoma. The pleura is more commonly affected by metastatic lesions, leading to thoracic effusion associated with lymphatic or vascular obstruction or due to altered vascular permeability. The most common primary tumor affecting the pleural surface is mesothelioma, which is relatively rare in veterinary patients. Mediastinal lymphoma in the cat appears to have a predilection for young (<2 years of age) cats, while thymoma tends to occur in older cats and dogs. Clinical complaints associated with mediastinal masses are often related to compression of adjacent structures by a mass lesion. Impingement on the trachea leads to labored respiration (on inspiration and/or expiration). Thymoma can cause difficult or abnormal swallowing due to compression of the esophagus, and if secondary myasthenia gravis is present, progressive weakness, esophageal dysfunction, or collapse can be noted. A mediastinal mass can also cause inspiratory difficulty or changes in bark or meow associated with damage to the recurrent laryngeal nerve. As discussed previously, cranial vena caval syndrome and Horner’s syndrome can be present. Neoplastic processes that affect the pleural space, both primary and metastatic, usually affect middle‐aged to older animals. Clinical complaints associated with malignant pleural effusion are usually respiratory difficulty and signs of poor health, including weight loss and lack of appetite. A mediastinal mass that puts pressure on the intrathoracic trachea can lead to stridor due to airway obstruction or from damage to the recurrent laryngeal nerve impacting laryngeal abduction. Obstruction of venous return by a mediastinal mass can lead to cranial vena cava syndrome, with edema of the head, neck, and front limbs. Impingement on the sympathetic trunk can lead to Horner’s syndrome (see Figure 7.9). Pleural effusion leads to a restrictive pattern of respiration with increased respiratory rate and dampening of heart and lung sounds. Pleural effusion or a cranial mediastinal mass can lead to decreased thoracic compressibility. Thoracic radiographic features of a mediastinal mass include dorsal deviation of the trachea (Figure 7.12) and widening of the mediastinum. Pleural effusion may or may not be present. Thoracic ultrasound is useful for identifying characteristics of mediastinal mass lesions and can guide aspiration for cytology. Pleural fluid cytology is often diagnostic for neoplasia, and polymerase chain reaction for antigen receptor rearrangement can be helpful in distinguishing thymoma from lymphoma (Lana et al. 2006). Mesothelioma is anticipated to result in pleural effusion and mass lesions are generally not visible on radiographs. Pleural effusion cytology is often difficult to interpret in such cases, because reactive mesothelial cells are encountered with a number of pleural disease processes and are easily mistaken for neoplastic cells. CT can sometimes identify pleural lesions and will help direct surgical biopsies. Animals with metastatic neoplasia can show evidence of nodular infiltrates or lymphadenopathy on radiographs after an effusion has been removed. Ultrasound or CT has improved the ability to detect lesions and also allows aspiration for diagnostic cytology. Figure 7.12 (a) Right lateral and (b) dorsoventral radiographs from a 7‐year‐old spayed female domestic short hair (FS DSH). There is a mild amount of pleural effusion and a soft tissue opacity in the cranial thorax, causing elevation and narrowing of the trachea. Ultrasound‐guided aspiration confirmed thymoma. Protocols using various combinations of drugs, including cyclophosphamide, vincristine, cytosine arabinoside, l‐asparaginase, mitoxantrone, and prednisolone, are recommended rather than single‐agent therapy for treating mediastinal lymphoma. Radiation therapy can also be pursued. Surgical resection is required for thymoma. No specific treatment is available for mesothelioma or metastatic neoplasia, although intracavitary cisplatin could be considered. One study of lymphoma in the cat reported a median survival time of 9 months with a 49% survival rate at 1 year using cyclophosphamide, vincristine, and prednisolone (Teske et al. 2002) while a protocol with lomustine, doxorubicin, vincristine, and prednisolone reported over 80% survival in FeLV+ cats with mediastinal or multicentric lymphoma (Horta et al. 2021). Median survival time for cats with mediastinal lymphoma was ~8 months. Surgical removal of a thymoma by thoracotomy or thoracoscopy can be associated with prolonged survival, although when myasthenia gravis and mega‐esophagus are present concurrently, a guarded prognosis must be offered. Pleural effusion associated with primary pulmonary neoplasia, mesothelioma, or metastatic neoplasia carries a grave prognosis. Pleural effusive diseases are categorized by the amount of protein in the fluid and cell count (see Chapter 2). After this initial characterization specific diagnostic tests are indicated to determine the most likely etiology of the effusion. Hydrothorax refers to a low‐protein, low‐cellularity fluid that accumulates within the thorax due to a disturbance in Starling forces, the hydrostatic and oncotic pressures of the interstitial and vascular spaces (Eq. 7.1):
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Pleural and Mediastinal Disease
Structural Disorders
Pneumothorax
Pathophysiology
History and Signalment
Physical Examination
Diagnostic Findings
Treatment
Prognosis
Pneumomediastinum
Pathophysiology
History and Signalment
Physical Examination
Diagnostic Testing
Treatment
Prognosis
Diaphragmatic Hernia
Pathophysiology
History and Signalment
Physical Examination
Diagnostic Findings
Treatment
Prognosis
Infectious Disorders
Pyothorax
Pathophysiology
History and Signalment
Physical Examination
Diagnostic Findings
Dog
Cat
Aerobes
17–22%
4–7%
37–57%
48–70%
19–22%
15–24%
Anaerobes
18–27%
20–34%
25%
24–48%
21–27%
17–45%
7–9%
10–12%
Treatment
Prognosis
Mediastinitis/Mass Effect/Hemorrhage
Pathophysiology
History and Signalment
Physical Examination
Diagnostic Testing
Treatment
Prognosis
Neoplastic Disorders
Pathophysiology
History and Signalment
Physical Examination
Diagnostic Findings
Treatment
Prognosis
Other Pleural Disorders
Hydrothorax
Pathophysiology
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