QUARTERLY BEAT / OCTOBER 2024
QUARTERLY BEAT / OCTOBER 2024
in distribution according to the underlying cause. Patterns are often asymmetric and related to the location of trauma that caused hemorrhage to occur. Although the pulmonary pattern is relatively nonspecific, numerous other thoracic radiographic changes are common, including pleural effusion, increased mediastinal soft tissue opacity or widening due to effusion or hematoma, tracheal narrowing, and tracheal collapse. 12,13 The presence of these other thoracic changes combined with an absence of cardiomegaly or pulmonary lobar venous enlargement makes differentiating hemorrhage from L-CHF easier than the aforementioned causes. METASTATIC NEOPLASIA Most neoplasms typically cause a structured interstitial pulmonary pattern when they metastasize to the lungs, resulting in multifocal pulmonary nodules or masses. However, lymphoma, hemangiosarcoma, and mammary adenocarcinoma commonly cause a patchy to diffuse, unstructured interstitial pulmonary pattern when they metastasize. The absence of obvious nodules/masses in the presence of an unstructured interstitial pulmonary pattern can be confusing if a patient presents for dyspnea and happens to have cardiomegaly as a normal breed variant or occult cardiac disease such as mitral valve degeneration. The key to differentiating diffuse pulmonary neoplasia from L-CHF is to identify other findings that would support a diagnosis of cancer. For example, finding a mammary mass in the case of mammary adenocarcinoma, finding a splenic/ hepatic masses, a hemoabdomen, or pericardial effusion in the case of hemangiosarcoma, or finding lymphadnomegaly, hepatosplenomegaly, visceral masses, or unexplained cavitary effusions in the case of lymphoma. As has been the theme, failure to respond to a furosemide trial is always an important clinical clue to rule out L-CHF.
cardiogenic pulmonary edema, pneumonia, and pulmonary hemorrhage. For this reason, a lack of radiographic improvement to other supportive therapies such as furosemide or antibiotics in the face of right sided cardiomegaly and pulmonary lobar artery enlargement should raise suspicion for PH. In contrast, acute improvement or resolution of pulmonary infiltrates with sildenafil is strongly supportive of PH and will not interfere with the diagnosis of the disease via echocardiography. 7 If patients develop right-sided CHF secondary to severe pulmonary hypertension, other radiographic findings may be seen, including pleural effusion, caudal vena cava enlargement, hepatomegaly, and peritoneal effusion. 4 While pulmonary hypertension is less commonly reported in cats, radiographic findings appear to be similar to those reported in the dog. CHRONIC LOWER AIRWAY DISEASE AND PULMONARY FIBROSIS Chronic lower airway disease is usually easily distinguished from L-CHF in that it primarily affects young to middle-aged dogs and cats and typically manifests radiographically as a mild to moderate bronchial pulmonary pattern without cardiomegaly. Early in the disease, pulmonary infiltrates are not seen and the cardiac silhouette and pulmonary lobar vasculature are expected to be normal. As the disease progresses, pulmonary infiltrates become more likely, usually resulting from concurrent pneumonia, pulmonary fibrosis, and/or pulmonary hypertension secondary to cor pulmonale. In the case of the later, right-sided cardiomegaly commonly occurs. Even more confusing, some dogs and cats will have stable/occult cardiac disease (mitral valve disease in dogs, cardiomyopathy in cats) that causes left-sided cardiomegaly. The presence of pulmonary infiltrates with or without cardiomegaly is when chronic lower airway disease can be confused with heart failure. As previously discussed, failure to respond radiographically to furosemide, a lack of pulmonary lobar venous congestion, a lack of cardiomegaly, or right-sided cardiomegaly should all decrease suspicion for L-CHF. Patients with chronic lower airway disease usually respond acutely well to bronchodilators and oxygen therapy.
neurogenic causes (e.g., seizures and head trauma), electrocution injury, anaphylaxis, toxin exposure, and acute lung injury. Regardless of the cause, NCPE presents as a multifocal to diffuse, unstructured interstitial or alveolar pulmonary pattern, often most severe in the periphery of the caudodorsal lung fields. A perihilar distribution is also reported. Pulmonary patterns are usually bilaterally symmetric, but can also be asymmetric. In one study, if the radiographic pattern was asymmetric, 86% of cases were most severe in the right caudodorsal lung field. 9 In that same study, the most common cause of an asymmetric pulmonary pattern was airway obstruction. The radiographic pattern itself is very similar to that associated with L-CHF. However, oftentimes patients are presented with a history that strongly supports a diagnosis of NCPE, such as dyspnea localized to the upper airways, near- drowning, seizures, or head trauma. Additional clues that decrease the likelihood of L-CHF include the absence of a heart murmur, cardiomegaly, or pulmonary lobar vasculature enlargement, as well as a lack of response to furosemide. PULMONARY THROMBOEMBOLISM Pulmonary thromboembolism (PTE) is uncommon in dogs and cats, but most often secondary to an underlying process that has disrupted Virchow’s triad of coagulation: stasis of blood flow, endothelial injury, and hypercoagulability. In veterinary medicine, underlying causes of PTE are numerous and well- reviewed elsewhere. 10 Idiopathic PTE is rare in dogs and cats. Unfortunately, radiographic findings are inconsistent and often not present. Depending on the size and number of vessels affected as well as the underlying cause, two main radiographic patterns are possible. Small or multifocal PTEs will cause a focal or multifocal unstructured interstitial or alveolar pulmonary pattern. 11 The pulmonary lobar arteries among or adjacent to this pattern will be small to absent. In contrast, if a large pulmonary lobar artery is affected, regional oligemia will cause hyper lucency and small to absent pulmonary lobar arteries within the affected lung lobe/region. Adjacent lung lobes/regions will receive increased blood flow, resulting in a patchy to diffuse unstructured interstitial pulmonary pattern with or without pulmonary lobar artery enlargement. Unfortunately, radiographs are often unremarkable and more advanced diagnostics are needed, such as radiographic or computed tomographic angiography. Pulmonary thromboembolism should be prioritized over L-CHF anytime a patient with a predisposing cause for PTE develops an acute but moderate to severe dyspnea (or even sudden death) in the face of underwhelming thoracic radiographic findings. PULMONARY HEMORRHAGE Pulmonary hemorrhage is uncommon in dogs and cats. When it occurs, it is most often caused by anti-coagulant rodenticide toxicity, other coagulopathies, thrombocytopenia, or large vessel rupture secondary to trauma. The pulmonary pattern associated with pulmonary hemorrhage is usually a patchy to diffuse, unstructured interstitial to alveolar pulmonary pattern that varies
6. Lee SK and Choi J. Caudal pulmonary artery to vein ratio on radiography can predict pulmonary hypertension in dogs with mitral regurgitation. Vet Radiol Ultrasound 2023;64(1): 18-27. 7. Kellihan HB, Waller KR, Pinkos A, et al. Acute resolution of pulmonary alveolar infiltrates in 10 dogs with pulmonary hypertension treated with sildenafil citrate: 2005-2014. J Vet Cardiol 2015;17(3):182-191. 8. Unger K and Martin LG. Noncardiogenic pulmonary edema in small animals (clinical practice review). J Vet Emerg and Crit Care 2023;33(2):156-172. 9. Bouyssou S, Specchi S, and Desquillbet et al. Radiographic appearance of presumed noncardiogenic pulmonary edema and correlation with the underlying cause in dogs and cats. Vet Radiol Ultrasound 2017;58(3):259-265. 10. Goggs R, Benigni L, and Fuentes VL, et al. Pulmonary thromboembolism (state-of-the-art review). J Vet Emerg Crit Care 2009;19(1):30-52. 11. Fluckiger MA and Gomez JA. Radiographic findings in dogs with spontaneous pulmonary thromboembolism. Vet Radiol Ultrasound 1984;25(3):124-131. 12. Berry CR, Gallaway A, Thrall De, et al. Thoracic radiographic features of anticoagulant rodenticide toxicity in fourteen dogs. Vet Radiol Ultrasound 1993;34(6):391-396. 13. Thomer AJ and Beer KAS. Anticoagulant rodenticide toxicosis causing tracheal collapse in 4 small breed dogs. J Vet Emerg Crit Care 2018;28(6):573-578.
ADDITIONAL REFERENCES
1. Bahr, R. Chapter 35: Canine and Feline Cardiovascular System. In: Thrall DE (eds). Textbook of Veterinary Diagnostic Radiology. 7th eds. St Louis, MO: Elsevier, 2018, pp 684 – 709. 2. Boysen SR. Chapter 189: AFAST and TFAST in the intensive care unit. In: Silverstein, DC and Hopper, K. Small Animal Critical Care Medicine, 2nd ed. 2015:988-994. 3. Dickson D, little CJL, Harris J, et al. Rapid assessment with physical examination in dyspnoeic cats: the RAPID cat study. J Small Anim Pract 2018;59:75-84. 4. Geyer NE, Reichle JK, Valdes-Martinez A, et al. Radiographic appearance of confirmed pulmonary lymphoma in cats and dogs. Vet Radiol Ultrasound 2010;51(4):386-390. 5. Guglielmini C, Toaldo MB, Poser H, et al. Diagnostic accuracy of the vertebral heart score and other radiographic indices in the detection of cardiac enlargement in cats with different cardiac disorders. J Fel Med Surg. 6. Lisciandro GR and Gambino JM (eds). Diagnostic imaging: point-of-care ultrasound. Vet Clin Smal Anim 2021;51(6). 7. Louvet A and Bourgeois, JM. Lung ring-down artifact as a sign of pulmonary alveolar-interstitial disease. J Vet Radiol Ultrasound 2008;49(4):374-377. 8. Sleeper MM, Roland R, and Drobatz KJ, et al. Use of the vertebral heart scale for differentiation of cardiac and noncardiac causes of respiratory distress in cats: 67 cases (2002-2003). J Am Vet Med Assoc 2013;242(3):366-371. 9. Thrall, DE. Chapter 36: Canine and Feline Lung. In: Thrall DE (eds). Textbook of Veterinary Diagnostic Radiology. 7th eds. St Louis, MO: Elsevier, 2018, pp 710 - 734.
SELECT REFERENCES
1. Cole L, Pivetta M, and Humm K. Diagnostic accuracy of a lung ultrasound protocol (VetBLUE) for detection of pleural fluid, pneumothorax and lung pathology in dogs and cats. J Small Anim Pract 2021;62(3):178-186. 2. Oura TJ, Young AN, Keene BW, et al. A valentine-shaped cardiac silhouette in feline thoracic radiographs is primarily due to left atrial enlargement. Vet Radiol Ultrasound 2015;56(3):245-250. 3. Reinero C, Visser LC, Kellihan HB, et al. ACVIM consensus statement guidelines for the diagnosis, classification, treatment, and monitoring of pulmonary hypertension in dogs. J Vet Intern Med 2020;34:549-573. 4. Johnson L, Boon J, and Orton EC. J Vet Intern Med 1999;13:440-447 5. Adams DS, Marolf AJ, and Martinez AV, et al. Associations between thoracic radiographic changes and severity of pulmonary arterial hypertension diagnosed in 60 dogs via Doppler echocardiography: A retrospective study: Vet Rad Ultrasound 2017;58(4):363-489.
NON-CARDIOGENIC PULMONARY EDEMA
Non-cardiogenic pulmonary edema (NCPE) is a less common cause of dyspnea in dogs and cats and includes any process that alters pulmonary vascular permeability. In some etiologies, aberrancies in hydrostatic pressure also play a role. The result is the accumulation of proteinaceous fluid within the interstitial or alveolar spaces without the presence of a cardiac or iatrogenic fluid therapy cause. 8 This is in contrast to cardiogenic pulmonary edema which causes non-proteinaceous fluid accumulation via increased hydrostatic pressure, most commonly caused by L-CHF, fluid therapy, or blood product administration. Causes of NCPE are numerous and include but are not limited to airway obstruction,
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