Underlying diseases in dogs referred to a veterinary teaching hospital because of dyspnea: 229 cases (2003–2007)

Sonja Fonfara Small Animal Teaching Hospital, School of Veterinary Science, University of Liverpool, Leahurst, Neston, CH64 7TE, England.

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Lourdes de la Heras Alegret Small Animal Teaching Hospital, School of Veterinary Science, University of Liverpool, Leahurst, Neston, CH64 7TE, England.

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Alexander J. German Small Animal Teaching Hospital, School of Veterinary Science, University of Liverpool, Leahurst, Neston, CH64 7TE, England.

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Laura Blackwood Small Animal Teaching Hospital, School of Veterinary Science, University of Liverpool, Leahurst, Neston, CH64 7TE, England.

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Joanna Dukes-McEwan Small Animal Teaching Hospital, School of Veterinary Science, University of Liverpool, Leahurst, Neston, CH64 7TE, England.

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P-J. M. Noble Small Animal Teaching Hospital, School of Veterinary Science, University of Liverpool, Leahurst, Neston, CH64 7TE, England.

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Rachel D. Burrow Small Animal Teaching Hospital, School of Veterinary Science, University of Liverpool, Leahurst, Neston, CH64 7TE, England.

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Abstract

Objective—To identify the most frequent underlying diseases in dogs examined because of dyspnea and determine whether signalment, clinical signs, and duration of clinical signs might help guide assessment of the underlying condition and prognosis.

Design—Retrospective case series.

Animals—229 dogs with dyspnea.

Procedures—Case records of dogs referred for dyspnea were reviewed and grouped according to location or etiology (upper airway, lower respiratory tract, pleural space, cardiac diseases, or obesity and stress). Signalment, clinical signs at initial examination, treatment, and survival time were analyzed.

Results—Upper airway (n = 74 [32%]) and lower respiratory tract (76 [33%]) disease were the most common diagnoses, followed by pleural space (44 [19%]) and cardiac (27 [12%]) diseases. Dogs with upper airway and pleural space disease were significantly younger than dogs with lower respiratory tract and cardiac diseases. Dogs with lower respiratory tract and associated systemic diseases were significantly less likely to be discharged from the hospital. Dogs with diseases that were treated surgically had a significantly better outcome than did medically treated patients, which were significantly more likely to be examined on an emergency basis with short duration of clinical signs.

Conclusions and Clinical Relevance—In dogs examined because of dyspnea, young dogs may be examined more frequently with breed-associated upper respiratory tract obstruction or pleural space disease after trauma, whereas older dogs may be seen more commonly with progressive lower respiratory tract or acquired cardiac diseases. Nontraumatic acute onset dyspnea is often associated with a poor prognosis, but stabilization, especially in patients with cardiac disease, is possible. Obesity can be an important contributing or exacerbating factor in dyspneic dogs.

Abstract

Objective—To identify the most frequent underlying diseases in dogs examined because of dyspnea and determine whether signalment, clinical signs, and duration of clinical signs might help guide assessment of the underlying condition and prognosis.

Design—Retrospective case series.

Animals—229 dogs with dyspnea.

Procedures—Case records of dogs referred for dyspnea were reviewed and grouped according to location or etiology (upper airway, lower respiratory tract, pleural space, cardiac diseases, or obesity and stress). Signalment, clinical signs at initial examination, treatment, and survival time were analyzed.

Results—Upper airway (n = 74 [32%]) and lower respiratory tract (76 [33%]) disease were the most common diagnoses, followed by pleural space (44 [19%]) and cardiac (27 [12%]) diseases. Dogs with upper airway and pleural space disease were significantly younger than dogs with lower respiratory tract and cardiac diseases. Dogs with lower respiratory tract and associated systemic diseases were significantly less likely to be discharged from the hospital. Dogs with diseases that were treated surgically had a significantly better outcome than did medically treated patients, which were significantly more likely to be examined on an emergency basis with short duration of clinical signs.

Conclusions and Clinical Relevance—In dogs examined because of dyspnea, young dogs may be examined more frequently with breed-associated upper respiratory tract obstruction or pleural space disease after trauma, whereas older dogs may be seen more commonly with progressive lower respiratory tract or acquired cardiac diseases. Nontraumatic acute onset dyspnea is often associated with a poor prognosis, but stabilization, especially in patients with cardiac disease, is possible. Obesity can be an important contributing or exacerbating factor in dyspneic dogs.

Dyspnea is defined as difficult or labored breathing and can result in severe physiologic compromise. Hypoxemia or hypercapnia can stimulate respiration, although under normal conditions, respiration is driven by an increase in carbon dioxide.1 Airway problems, primary or secondary lung parenchymal diseases, or pleural space diseases are frequent causes of dyspnea.1

Definitive treatment of dyspnea depends on the underlying cause.1,2 Breed conformational problems, airway occlusion, and pleural space diseases are often surgically managed with excellent outcome.3–8 Dyspnea associated with lung parenchymal, cardiac, or other systemic diseases is medically managed,1,2,9–12 and outcome depends on the severity of the underlying disease process and response to treatment, and may often have a poor prognosis.1,2,6,11,13

Given the range of possible causes and treatments in patients examined because of dyspnea, it is essential that a definitive diagnosis is made early. However, in the emergency setting, investigations are often hampered by the condition of the patient and, initially, only a tentative diagnosis and preliminary therapeutic plan may be possible. Especially in patients for which the history is not available, knowledge of age and breed predisposition (eg, brachycephalic breeds) and common underlying causes will help rapid and efficient management of patients with dyspnea. Therefore, the objectives of the study reported here were to identify the most frequent underlying diseases in dogs initially examined because of dyspnea and to determine whether signalment, nature, and duration of clinical signs might help in assessment of the possible underlying condition and prognosis.

Materials and Methods

Patients and records—The medical records of all dogs referred to the University of Liverpool Small Animal Teaching Hospital between January 2003 and December 2007 were searched for the term dyspnoea by use of a database software program.14,a Dogs were included if they were reported to be dyspneic on examination by the referring veterinarian or on initial examination at the University of Liverpool Hospital and if the case records included details on signalment, emergency or routine case, duration of clinical signs prior to examination, etiology of dyspnea, treatment, and euthanasia, death, or discharge from the hospital. To assess for breed predispositions in the dyspneic patient population, breed frequencies were compared with those of the total hospital database by use of a database software program.b

For the purpose of analysis, dogs were assigned to 1 of 5 groups. The upper airway disease group included BOAS, laryngeal paralysis, tracheal collapse, and neoplasia. The lower respiratory tract disease group included pulmonary parenchymal disease (inflammatory, infectious, and neoplastic), noncardiogenic pulmonary edema, bronchial disease, PTE, DIC, ARDS, and coagulopathies. The pleural space disease group included pleural effusion (idiopathic, secondary to systemic disease or lung lobe torsion, and neoplastic), pneumothorax, pyothorax, neoplasia (thymoma and thymic and ectopic thyroid carcinoma), and PPDH. The cardiac disease group included acquired and congenital cardiac diseases causing pulmonary edema, pleural effusion, or both and pericardial effusion (idiopathic and neoplastic) associated with pleural effusion. The obesity or stress group included dogs where no underlying disease was detected. Body condition was assessed by use of the 9-point body condition scoring system,15 with patients with scores of 7/9 to 9/9 being considered overweight.

Diagnostic investigations and treatment—In all patients, physical examination, routine hematologic and serum biochemical analyses, and thoracic radiography or computed tomography of the thorax were performed. An arterial blood gas sample was analyzedc in some patients. When a lower respiratory cause was suspected, bronchoscopy and bronchoalveolar lavage were performed and samples were sent for routine cytologic and bacteriologic examination. In dogs with pleural effusion, pneumothorax, or pyothorax, diagnostic and therapeutic thoracocentesis was performed; in these patients, fluid cytologic analysis and bacteriologic culture were conducted whenever an infectious cause was suspected. In patients with suspected coagulation abnormalities, a hemostatic profile (including prothrombin time, activated partial thromboplastin time, and measurement of fibrinogen concentration and fibrinogen degradation products) was performed and, in some patients, plasma D-dimer concentrations were measured.d In patients with an accessible thoracic mass, thoracic ultrasonography was performed and diagnosis was obtained by either fine-needle aspiration for cytologic analysis or soft tissue biopsies for histologic examination. Dogs with cardiac disease underwent blood pressure measurement, 6-lead ECG, and echocardiography. Supportive treatment was initiated in all unstable dogs, and diagnostic tests were only performed when the patient was stable. Severely dyspneic dogs received supplemental oxygen on initial examination. Further treatment depended on the underlying condition. Medical treatment included bronchodilators, diuretics, antimicrobials, anti-inflammatory drugs, various chemotherapy protocols, vasodilators, positive inotropic drugs, antifibrotic drugs (eg, colchicine), vasopressors, blood or plasma transfusions, and thrombolytic agents. In patients with pleural space diseases causing dyspnea, thoracocentesis was performed as required. Surgery was performed in patients with structural or obstructive airway diseases, pleural space disease, and neoplasia if indicated.

Statistical analysis—Data were entered into spreadsheets,e and statistical analysis was performed with a commercial software package.f Data were expressed with simple descriptive statistics (mean, median, variance, SD, interquartile range, and confidence interval). Comparison between breeds, age of animals, groups, duration of clinical signs, initial examination as emergency or routine case, and likelihood of discharge were compared by use of a Kruskal-Wallis test for ≥ 3 groups and Mann-Whitney U tests for comparison of 2 groups. The proportion of breeds in the overall patient population was compared with the dyspneic population for the most common breeds by use of a χ2 test. To compare the duration of clinical signs before initial evaluation in different age groups, animals were assigned to 1 of 4 groups: ≤ 1.5 years old, > 1.5 to 5 years old, > 5 to 9 years old, and > 9 years old. Death and euthanasia were not classified as separate outcomes because euthanasia was invariably performed because of severe clinical signs, progression of disease, or failure to respond to treatment. Values of P < 0.05 were considered significant.

Results

Of 13,293 referred new patients, 229 (1.7%) dogs had dyspnea as the main clinical sign for the study period. A range of breeds were included, with Bulldogs (n = 22), Labrador Retrievers (20), mixed breeds (19), and Cavalier King Charles Spaniels (19) being most common. In comparison to the hospital population, Bulldogs (P < 0.001), Cavalier King Charles Spaniels (P < 0.001), Staffordshire Bull Terriers (P = 0.016), Yorkshire Terriers (P = 0.028), and Pugs (P < 0.001) were significantly overrepresented in the dyspneic population. The median age of all dyspneic dogs was 6 years (interquartile range, 2 to 9 years). Bulldogs, Jack Russell Terriers, Dogues de Bordeaux, English Springer Spaniels, and Rottweilers were significantly (P < 0.001) younger (median age, < 2 years; interquartile range, 1 to 4 years), whereas mixed-breed dogs, Yorkshire Terriers, German Shepherd Dogs, Doberman Pinschers, Greyhounds, Golden Retrievers, and Poodles were significantly (P < 0.001) older (median age, > 8 years; interquartile range, 6 to 10 years; Table 1) than other breeds examined because of dyspnea.

Table 1—

Underlying diseases in dogs (n = 229) referred to a veterinary teaching hospital because of dyspnea.

GroupEtiologyNo. (%)Age(y [interquartile range])Examined as emergency case (No.)Surgery (No. [%])Discharged (No. [%])
Upper airway disease (n = 74 [32%])BOAS39 (53)2 (1–5)1231 (79.5)33 (84.6)
 Laryngeal paralysis22 (30)9.5 (6.5–12)141817
 Tracheal collapse10 (14)6.5 (4.25–11)506
Lower respiratory tract disease (n = 76 [33%])Neoplasia31 (41)8 (6–9)1907
 PTE14 (18)6 (3.75–7.25)1404
 Bacterial bronchopneumonia10 (13)3.5 (0.85–7.75)1004
 Lung bullae7 (9)7 (1–10)575
 Pulmonary fibrosis5 (6.6)12 (4.5–13.5)202
 Alveolar, interstitial lung pattern*5 (6.6)5 (1.6–7.5)500
 ARDS2 (2.6)1 and 11201
Pleural space disease (n = 44 [19%])Pleural effusion15 (34)4 (1.75–6.25)888
 Pneumothorax13 (30)2 (1–4)11611
 Pyothorax8 (18)3.5 (1.25–6.75)724
 Neoplasia6 (14)8.5 (6.75–10.25)633
Cardiac disease (n = 27 [12%])DCM9 (33)6 (5–9)907
 DVD9 (33)7 (6.5–10.5)906
 MD and AS3 (11)1 (0.5–6)303
 Pericardial effusion4 (15)8 (4–10.5)202
Obesity and stress (n = 8 [4%])Obesity47.5 (4.75–8.0)104
 Stress45.5 (4.25–6.75)204

Alveolar or interstitial lung pattern was identified on thoracic radiographs, but no diagnosis was made because further diagnostic investigations were not possible because of severity of clinical signs and these dogs died or were euthanized within the first 24 hours.

AS = Aortic valve stenosis. MD = Mitral valve dysplasia.

Most dogs had upper airway (n = 74 [32%]) or lower respiratory tract disease (76 [33%]), followed by pleural space (44 [19%]) and cardiac diseases (27 [12%]) as the cause of dyspnea; however, a small group of dogs had dyspnea because of obesity combined with stress (n = 8 [4%]; Table 1). One hundred thirty-five of 229 (60%) dogs were discharged from the hospital.

Upper airway diseases—Dogs in the upper airway disease group were examined because of BOAS (n = 39 [53%]), laryngeal paralysis (22 [30%]), and tracheal collapse (10 [14%]; Table 1). Most dogs examined because of BOAS were Bulldogs (n = 16), Pugs (7), Cavalier King Charles Spaniels (5), Staffordshire Bull Terriers (4), and Dogues de Bordeaux (2). They were significantly (P < 0.001) younger (median age, 2 years; interquartile range, 1 to 5 years) than the other dogs in this group (median age, > 9 years; interquartile range, 5 to 11 years), and 7 (18%) of these dogs were obese. Two of the dogs with BOAS died within the first 4 hours after evaluation; one dog regurgitated and then aspirated leading to asphyxiation, and the other dog died because of complications of surgery performed by the referring veterinarian. A further 4 dogs died during anesthesia for or recovery from corrective surgery.

Dogs examined because of laryngeal paralysis were mainly large breeds, including 5 mixed breeds, 4 Labrador Retrievers, and 3 English Bull Terrier; in contrast, dogs with tracheal collapse were small breeds (5 Yorkshire Terriers and 2 Toy Poodles).

Lower respiratory tract diseases—Dogs in the lower respiratory tract disease group were initially examined because of neoplasia (n = 31 [41%]), PTE (14 [18%]), bacterial bronchopneumonia (10 [13%]), lung bullae (7 [9%]), pulmonary fibrosis (5 [6.6%]), alveolar or interstitial lung pattern on thoracic radiographs taken at evaluation, and suspected ARDS (2 [2.6%]; Table 1). For the dogs in which alveolar or interstitial lung pattern on thoracic radiographs was listed without a diagnosis, further diagnostic investigations were not possible because of severity of clinical signs and these dogs died or were euthanized within the first 24 hours. Sixteen of the dogs with neoplasia had a diagnosis of lymphoma, 6 dogs had primary or metastatic pulmonary adenocarcinoma, and 4 dogs had histiocytic sarcoma or malignant histiocytosis (3 of these were Bullmastiffs, and the other dog was a Flat-Coated Retriever). In 5 dogs, a lung mass was present but a final diagnosis was not achieved because the owners declined further investigations. Dogs with neoplasia (median age, 8 years; interquartile range, 6 to 9 years) were not older than dogs with other lower respiratory tract diseases (median age, 6 years; interquartile range, 3 to 9.5 years; P = 0.13). However, dogs with lymphoma (median age, 6 years; interquartile range, 2 to 8 years) were significantly (P = 0.008) younger than dogs with other types of neoplasia (median age, 9 years; interquartile range, 7 to 10 years). All dogs with systemic histiocytic diseases or a lung mass of unknown etiology died or were euthanized within 1 month after evaluation, as were 4 of the dogs with pulmonary adenocarcinoma and 11 of the patients with lymphoma.

Four dogs with PTE (n = 14) had a diagnosis of IMHA, and DIC was present in 2 of these patients. Breeds most commonly affected with PTE were mixed breeds (n = 4) and Greyhounds (3). Ten of 14 died or were euthanized within 4 days after initial examination, including all of the dogs with IMHA.

Two of the dogs with bacterial bronchopneumonia were Cavalier King Charles Spaniels and were diagnosed with Pneumocystis carinii infection. Four of 5 dogs with pulmonary fibrosis were West Highland White Terriers, 2 of which were discharged but subsequently euthanized after 2 months.

One 11-year-old West Highland White Terrier with suspected ARDS died shortly after admission, whereas one 1-year-old Jack Russell Terrier was successfully treated and discharged.

Pleural space diseases—Dogs with pleural space disease were examined with various types of pleural effusion (n = 15), pneumothorax (13), pyothorax (8), and neoplasia (6; Table 1). Seven of these dogs (including 2 Labrador Retrievers, 2 Bullmastiffs, and 2 Staffordshire Bull Terriers) had a diagnosis of idiopathic chylothorax, lung lobe torsion was identified in 2 dogs; 2 dogs had pleural effusion secondary to hypoalbuminemia (one dog because of a portosystemic shunt and the other because of protein-losing enteropathy), 1 had a PPDH, and 1 had sepsis. Surgical management was undertaken in all dogs with lung lobe torsion, in 5 of the dogs with idiopathic chylothorax, and in the single dog with PPDH. The dog with sepsis, the dogs with hypoalbuminemia, and 4 dogs with idiopathic chylothorax all died or were euthanized within 48 hours after admission.

Nine dogs with pneumothorax had a history of trauma, and a further 2 dogs developed pneumothorax following drainage of a pleural effusion. These dogs (median age, 2 years; interquartile range, 1 to 4 years) were significantly (P = 0.027) younger than the other dogs in this group (median age, 5 years; interquartile range, 2 to 7 years; Table 1). Duration of clinical signs before initial examination was significantly (P = 0.005) shorter (median, 1 day; interquartile range, 1 to 12 days) than in the other dogs in this group (median, 14 days; interquartile range, 5 to 25 days).

Neoplastic disease, including thymoma (n = 4) or thyroid carcinoma (2), was identified in a number of dogs in this group. Three of these dogs were Golden Retrievers, and 2 were Labrador Retrievers. These dogs were significantly (P = 0.001) older than the other dogs in this group (Table 1). Three dogs were discharged from the hospital (2 of them after surgical treatment), but all dogs died or were euthanized within 6 weeks after admission.

Cardiac diseases—Dogs in the cardiac disease group were initially examined because of acquired cardiac diseases (n = 18), congenital cardiac diseases (3), and pericardial effusion (4; Table 1). As expected, dogs with DVD were mainly small-breed dogs (6 Cavalier King Charles Spaniels but also 2 German Shepherd Dogs), whereas dogs with DCM were large-breed dogs (4 Doberman Pinschers, 1 Great Dane, 1 Irish Wolfhound, and 1 Labrador Retriever). There was no significant (P = 0.11) difference in age between these groups of dogs (dogs with DVD [median age, 7 years; interquartile range, 6.5 to 10.5 years] and dogs with DCM [median age, 6 years; interquartile range, 5 to 9 years]). Furthermore, duration of clinical signs was not significantly (P = 0.11) different between dogs with DVD (median, 2 days; interquartile range; 1 to 5 days) and dogs with DCM (median, 7 days; interquartile range, 2 to 14 days).

Of the dogs in this group that were discharged, median survival time to death or euthanasia was 150 days (interquartile range, 37 to 195 days) for dogs with DCM and 90 days (interquartile range, 19 to 337 days) for dogs with DVD (P = 1.0). The cause of dyspnea was thought to be arrhythmogenic right ventricular cardiomyopathy in 1 Boxer and a tachycardiomyopathy causing congestive heart failure in 1 Bulldog. Two English Bull Terriers, which were < 1 year old, and 1 Labrador Retriever, which was 7 years old, were evaluated because of mitral valve dysplasia and aortic valve stenosis. These dogs were discharged after treatment but were euthanized within the next 4 months. In 2 dogs with pericardial and pleural effusion, cardiac neoplasia was detected, and they were euthanized. Another dog was euthanized 1 week later after recurrence of pericardial effusion.

Stress and obesity—Dogs examined because of dyspnea but in which no underlying disease was detected improved with supplemental oxygen and additional supportive treatment. Four of these patients were obese small-breed dogs (1 each of Jack Russell Terrier, Cavalier King Charles Spaniel, Yorkshire Terrier, and Bulldog), and all had a long duration of clinical signs (median, 150 days; interquartile range, 62 to 450 days). The other 4 dogs were classified as having stress-related dyspnea (1 each of Bulldog, Boxer, Newfoundland, and Labrador Retriever).

Comparison among groups—One hundred fifty-four of the 229 (67%) dogs with dyspnea were examined as emergency referrals, with dogs with cardiac disease, pleural space disease, and lower respiratory tract disease being more likely to be examined on an emergency basis (P = 0.001).

Dogs with upper airway (median age, 5 years; interquartile range, 1.5 to 9 years) and pleural space (median age, 4 years; interquartile range, 2 to 7 years) disease were significantly (P = 0.018) younger than dogs with lower respiratory tract (median age, 7 years; interquartile range, 3 to 9 years) and cardiac disease (median age, 7 years; interquartile range, 5 to 9 years). Duration of clinical signs was significantly (P < 0.001) different between groups, with dogs with cardiac diseases (median, 3 days; interquartile range, 1 to 8 days) having the shortest duration and dogs with upper airway diseases (median, 49 days; interquartile range, 20.75 to 180 days) and obesity- or stress-related dyspnea (median, 25 days; interquartile range, 1 to 165 days) having the longest duration of clinical signs. Likelihood of discharge from the hospital was also significantly (P < 0.001) different among groups. However, there was no significant (P = 0.075) difference in the duration of clinical signs among the age groups. Perhaps not surprisingly, duration of clinical signs was significantly (P < 0.001) shorter in dogs examined as emergency referrals (median, 5 days; interquartile range, 2 to 21 days) than in dogs examined as routine cases (median, 42 days; interquartile range, 21 to 180 days). However, duration of clinical signs in dogs requiring surgical management (median, 42 days; interquartile range, 10 to 76 days) was significantly (P < 0.001) longer than in dogs that were managed medically (median, 7 days; interquartile range, 2 to 21 days) and a lower proportion were examined on an emergency basis (41/76 [54%] vs 118/153 [77%], respectively; P = 0.007). Furthermore, a greater proportion of dogs (62/76 [82%]) that underwent surgical management were discharged than those receiving medical treatment (74/153 [48%]; P < 0.001).

Discussion

The results of the present study showed, not surprisingly, an overrepresentation of dogs with breed-conformational upper airway problems, which result in changes to the normal respiratory strategy.16 Most (67%) dogs with dyspnea were examined on an emergency basis, and only 60% of these patients were discharged from the hospital, confirming that dyspnea reflects major respiratory compromise with a high potential for a negative outcome.

Similar numbers of dogs were examined with upper airway (n = 74) and lower respiratory tract disease (76). Dogs with conformational problems of the upper airway were easily identified by their brachycephalic breed and younger age.3,16,17 Most of them were referred as routine cases, which is consistent with longer duration of clinical signs before initial examination and a better outcome for this group than for patients with other causes of dyspnea, likely because surgery significantly improves outcome.3 In contrast, dogs with lower respiratory tract disease were older and had an acute onset of clinical signs, perhaps related to the etiologies (eg, neoplasia) seen in this group. However, whereas age can help to predict etiology, this should not be the sole criterion for decision making, as highlighted by the finding that dogs with lymphoma were examined at a significantly younger age, as has been reported previously.18 The poor outcome in the lower respiratory tract disease group in the present study is likely to be related to the etiologies seen, given that neoplasia was common as well as other diseases with a known poor prognostic outcome (eg, pulmonary fibrosis and PTE).10,11,13,19 Furthermore, dogs have an excellent collateral ventilation, which protects against airway obstruction; however, the ability to redistribute blood flow from poorer- to better-ventilated regions of the lung may be limited.20 Dyspnea is therefore likely to be associated with marked impairment of lung function.

Interestingly, the present study did not identify many dogs initially examined because of bacterial bronchopneumonia, perhaps because this condition is uncommon or is successfully managed in a primary care setting. All such patients (n = 10) were examined on an emergency basis, and 6 died or were euthanized, suggesting that patients with refractory or severe disease were more likely to be referred.

In the present study, patients with cardiac disease had a short duration of clinical signs and were examined on an emergency basis, likely because of the finding that acquired cardiac disease predominated, with obvious clinical signs (eg, heart murmur and arrhythmias).9,21–23 Not surprisingly, Cavalier King Charles Spaniels, reported24,25 to be predisposed to DVD, were overrepresented in the dyspnea population and in this group in the present study.

Most patients in the present study with diseases which could be treated with surgery (BOAS, laryngeal paralysis, lung lobe bullae, traumatic pneumothorax, and idiopathic pleural effusion) had a favorable outcome, as previously reported.3–5,7,8 This is consistent with treatment of breed-associated conformational or acquired problems, which can be improved with surgery.3–5,7,8,16 The longer duration of clinical signs before initial examination and referral as a routine visit suggests adaptation of these dogs to their condition, a slow progression of disease, or both. However, acute decompensation (eg, in a stressful situation) and emergency examination of a previously stable patient is possible and should not be underestimated.26

Medically treated patients either had conditions that were not amenable to surgery, had severe lung disease resulting in acute progression and decompensation, had associated systemic disease (IMHA, DIC, or ARDS), or had conditions potentially amenable to surgery but were too unstable. These conditions are often associated with poor response to treatment and prognosis and an owner's decision for euthanasia, as has been reported previously,1,2,6 and the number of dogs discharged with medically treated diseases was significantly lower in the present study. However, stabilization of a patient with decompensated cardiac disease was often possible, which has been reported previously.12,24,27,28

Obesity was considered to be an important factor contributing to clinical signs in dogs with BOAS and tracheal collapse. Interestingly, in 8 patients in the present study, obesity with or without stress was considered to be the cause of dyspnea. As expected, these patients had a long (median, 150 days) duration of clinical signs when initially examined. Not all obese patients develop dyspnea, but reduced compliance of the respiratory system, increases in airway or pulmonary resistance, and reduced respiratory muscle strength result in changes in respiratory strategy and reduced ability to respond to heat and stress,26,29 which were frequently noted in the history of obese dyspneic dogs in the present study. The association among obesity, upper airway obstruction, and impaired lung function has been established in studies in humans29,30 and in a study of dogs with BOAS.16 Weight loss should therefore be considered important in the long-term management of obese dyspneic veterinary patients.

Limitations of the present study include the problems common to all retrospective studies. First, such studies are reliant on accuracy of clinical records and recording of data. Further, the investigations and treatment performed at the time could have been limited by nonclinical factors (eg, financial constraints). Because this was a referral population, diseases such as upper and lower respiratory tract infections are likely to be underrepresented and only small numbers of infectious diseases were present. The proportion of emergency cases was likely to be higher. Long-term follow-up was not obtained, and instead, only survival to discharge was recorded. Finally, a wide variety of etiologies were represented, such that caution must be exercised in generalizing the findings to all patients with dyspnea. Therefore, our findings should be confirmed with prospective studies, ideally of single disease etiologies.

ABBREVIATIONS

ARDS

Acute respiratory distress syndrome

BOAS

Brachycephalic obstructive airway syndrome

DCM

Dilated cardiomyopathy

DIC

Disseminated intravascular coagulation

DVD

Degenerative valvular disease

IMHA

Immune-mediated hemolytic anemia

PPDH

Peritoneopericardial diaphragmatic hernia

PTE

Pulmonary thromboembolism

a.

ACTools, Animalcare, Intellisoft UK Ltd, Manchester, England.

b.

Tristan Veterinary Software, Aberdeen, Scotland.

c.

iSTAT analyzer, Heska Corp, Waukesha, Wis.

d.

Cambridge Specialists Laboratory Services, Cambridge, England.

e.

Microsoft Office Excel 2007, Microsoft Corp, Redmond, Wash.

f.

Minitab 15, Minitab Inc, State College, Pa.

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    Borgarelli M, Tarducci A, Tidholm A, et al. Canine idiopathic dilated cardiomyopathy. Part II: pathophysiology and therapy. Vet J 2001; 162: 182195.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 13.

    Dahl K, Gamlem H, Tverdal A, et al. Canine vascular neoplasia—a population-based study of prognosis. APMIS Suppl 2008; 125: 5562.

  • 14.

    Swift S, Dukes-McEwan J, Fonfara S, et al. Aetiology and outcome in 90 cats presenting with dyspnoea in a referral population. J Small Anim Pract 2009; 50: 466473.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 15.

    Laflamme DP. Development and validation of a body condition score system for dogs. Canine Pract 1997; 22(4):1015.

  • 16.

    Bernaerts F, Talavera J, Leemans J, et al. Description of original endoscopic findings and respiratory functional assessment using barometric whole-body plethysmography in dogs suffering from brachycephalic airway obstruction syndrome. Vet J 2010; 183: 95102.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 17.

    Wykes PM. Brachycephalic airway obstructive syndrome. Probl Vet Med 1991; 3: 188197.

  • 18.

    Gamlem H, Nordstoga K, Glattre E. Canine neoplasia—introductory paper. APMIS Suppl 2008; 125: 518.

  • 19.

    Liptak JM, Kamstock DA, Dernell WS, et al. Cranial mediastinal carcinomas in nine dogs. Vet Comp Oncol 2008; 6: 1930.

  • 20.

    Kirschvink N, Reinhold P. Use of alternative animals as asthma models. Curr Drug Targets 2008; 9: 470484.

  • 21.

    Borgarelli M, Zini E, D'Agnolo G, et al. Comparison of primary mitral valve disease in German Shepherd dogs and in small breeds. J Vet Cardiol 2004; 6: 2734.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 22.

    Tidholm A, Haggstrom J, Borgarelli M, et al. Canine idiopathic dilated cardiomyopathy. Part I: aetiology, clinical characteristics, epidemiology and pathology. Vet J 2001; 162: 92107.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 23.

    Wess G, Schulze A, Butz V, et al. Prevalence of dilated cardiomyopathy in Doberman Pinschers in various age groups. J Vet Intern Med 2010; 24: 533538.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 24.

    Borgarelli M, Savarino P, Crosara S, et al. Survival characteristics and prognostic variables of dogs with mitral regurgitation attributable to myxomatous valve disease. J Vet Intern Med 2008; 22: 120128.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 25.

    Borgarelli M, Zini E, D'Agnolo G, et al. Comparison of primary mitral valve disease in German Shepherd Dogs and in small animal breeds. J Vet Cardiol 2004; 6: 2734.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 26.

    Jensen D, Ofir D, O'Donnell DE. Effects of pregnancy, obesity and aging on the intensity of perceived breathlessness during exercise in healthy humans. Respir Physiol Neurobiol 2009; 167: 87100.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 27.

    Haggstrom J, Boswood A, OGrady M, et al. Effect of pimobendan or benazepril hydrochloride on survival times in dogs with congestive heart failure caused by naturally occuring myxomatous mitral valve disease: the QUEST study. J Vet Intern Med 2008; 22: 11241135.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 28.

    Haggstrom J, Hoglund K, Borgarelli M. An update on treatment and prognostic indicators in canine myxomatous mitral valve disease. J Small Anim Pract 2009; 50 (suppl 1): 2533.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 29.

    Parameswaran K, Todd DC, Soth M. Altered respiratory physiology in obesity. Can Respir J 2006; 13: 203210.

  • 30.

    Piper AJ, Grunstein RR. Big breathing: the complex interaction of obesity, hypoventilation, weight loss, and respiratory function. J Appl Physiol 2010; 108: 199205.

    • Crossref
    • Search Google Scholar
    • Export Citation
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    Tseng LW, Waddell LS. Approach to the patient in respiratory distress. Clin Tech Small Anim Pract 2000; 15: 5362.

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    Rozanski EA, Rondeau MP. Respiratory pharmacotherapy in emergency and critical care medicine. Vet Clin North Am Small Anim Pract 2002; 32: 10731086.

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    Riecks TW, Birchard SJ, Stephens JA. Surgical correction of brachycephalic syndrome in dogs: 62 cases (1991–2004). J Am Vet Med Assoc 2007; 230: 13241328.

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    Carobbi B, White RA, Romanelli G. Treatment of idiopathic chylothorax in 14 dogs by ligation of the thoracic duct and partial pericardiectomy. Vet Rec 2008; 163: 743745.

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    Fossum TW, Mertens MM, Miller MW, et al. Thoracic duct ligation and pericardectomy for treatment of idiopathic chylothorax. J Vet Intern Med 2004; 18: 307310.

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    Mellanby RJ, Villiers E, Herrtage ME. Canine pleural and mediastinal effusions: a retrospective study of 81 cases. J Small Anim Pract 2002; 43: 447451.

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    Lipscomb VJ, Hardie RJ, Dubielzig RR. Spontaneous pneumothorax caused by pulmonary blebs and bullae in 12 dogs. J Am Anim Hosp Assoc 2003; 39: 435445.

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    Puerto DA, Brockman DJ, Lindquist C, et al. Surgical and nonsurgical management of and selected risk factors for spontaneous pneumothorax in dogs: 64 cases (1986–1999). J Am Vet Med Assoc 2002; 220: 16701674.

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    Atkins C, Bonagura J, Ettinger S, et al. Guidelines for the diagnosis and treatment of canine chronic valvular heart disease. J Vet Intern Med 2009; 23: 11421150.

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    Corcoran BM, Cobb M, Martin MW, et al. Chronic pulmonary disease in West Highland white terriers. Vet Rec 1999; 144: 611616.

  • 11.

    Goggs R, Benigni L, Fuentes VL, et al. Pulmonary thromboembolism. J Vet Emerg Crit Care (San Antonio) 2009; 19: 3052.

  • 12.

    Borgarelli M, Tarducci A, Tidholm A, et al. Canine idiopathic dilated cardiomyopathy. Part II: pathophysiology and therapy. Vet J 2001; 162: 182195.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 13.

    Dahl K, Gamlem H, Tverdal A, et al. Canine vascular neoplasia—a population-based study of prognosis. APMIS Suppl 2008; 125: 5562.

  • 14.

    Swift S, Dukes-McEwan J, Fonfara S, et al. Aetiology and outcome in 90 cats presenting with dyspnoea in a referral population. J Small Anim Pract 2009; 50: 466473.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 15.

    Laflamme DP. Development and validation of a body condition score system for dogs. Canine Pract 1997; 22(4):1015.

  • 16.

    Bernaerts F, Talavera J, Leemans J, et al. Description of original endoscopic findings and respiratory functional assessment using barometric whole-body plethysmography in dogs suffering from brachycephalic airway obstruction syndrome. Vet J 2010; 183: 95102.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 17.

    Wykes PM. Brachycephalic airway obstructive syndrome. Probl Vet Med 1991; 3: 188197.

  • 18.

    Gamlem H, Nordstoga K, Glattre E. Canine neoplasia—introductory paper. APMIS Suppl 2008; 125: 518.

  • 19.

    Liptak JM, Kamstock DA, Dernell WS, et al. Cranial mediastinal carcinomas in nine dogs. Vet Comp Oncol 2008; 6: 1930.

  • 20.

    Kirschvink N, Reinhold P. Use of alternative animals as asthma models. Curr Drug Targets 2008; 9: 470484.

  • 21.

    Borgarelli M, Zini E, D'Agnolo G, et al. Comparison of primary mitral valve disease in German Shepherd dogs and in small breeds. J Vet Cardiol 2004; 6: 2734.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 22.

    Tidholm A, Haggstrom J, Borgarelli M, et al. Canine idiopathic dilated cardiomyopathy. Part I: aetiology, clinical characteristics, epidemiology and pathology. Vet J 2001; 162: 92107.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 23.

    Wess G, Schulze A, Butz V, et al. Prevalence of dilated cardiomyopathy in Doberman Pinschers in various age groups. J Vet Intern Med 2010; 24: 533538.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 24.

    Borgarelli M, Savarino P, Crosara S, et al. Survival characteristics and prognostic variables of dogs with mitral regurgitation attributable to myxomatous valve disease. J Vet Intern Med 2008; 22: 120128.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 25.

    Borgarelli M, Zini E, D'Agnolo G, et al. Comparison of primary mitral valve disease in German Shepherd Dogs and in small animal breeds. J Vet Cardiol 2004; 6: 2734.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 26.

    Jensen D, Ofir D, O'Donnell DE. Effects of pregnancy, obesity and aging on the intensity of perceived breathlessness during exercise in healthy humans. Respir Physiol Neurobiol 2009; 167: 87100.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 27.

    Haggstrom J, Boswood A, OGrady M, et al. Effect of pimobendan or benazepril hydrochloride on survival times in dogs with congestive heart failure caused by naturally occuring myxomatous mitral valve disease: the QUEST study. J Vet Intern Med 2008; 22: 11241135.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 28.

    Haggstrom J, Hoglund K, Borgarelli M. An update on treatment and prognostic indicators in canine myxomatous mitral valve disease. J Small Anim Pract 2009; 50 (suppl 1): 2533.

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 29.

    Parameswaran K, Todd DC, Soth M. Altered respiratory physiology in obesity. Can Respir J 2006; 13: 203210.

  • 30.

    Piper AJ, Grunstein RR. Big breathing: the complex interaction of obesity, hypoventilation, weight loss, and respiratory function. J Appl Physiol 2010; 108: 199205.

    • Crossref
    • Search Google Scholar
    • Export Citation

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