Biophysical properties of alveolar surfactant in drever dogs with hunting associated pulmonary edema.

BACKGROUND: A syndrome of acute non-cardiogenic pulmonary edema associated with hunting is prevalent in the drever breed, but etiology of this syndrome is currently unknown. Alveolar surfactant has a critical role in preventing alveolar collapse and edema formation. The aim of this study was to investigate, whether the predisposition to hunting associated pulmonary edema in drever dogs is associated with impaired biophysical properties of alveolar surfactant. Seven privately owned drever dogs with recurrent hunting associated pulmonary edema and seven healthy control dogs of other breeds were included in the study. All affected dogs underwent thorough clinical examinations including echocardiography, laryngeal evaluation, bronchoscopy, and bronchoalveolar lavage (BAL) as well as head, neck and thoracic computed tomography imaging to rule out other cardiorespiratory diseases potentially causing the clinical signs. Alveolar surfactant was isolated from frozen, cell-free supernatants of BAL fluid and biophysical analysis of the samples was completed using a constrained sessile drop surfactometer. Statistical comparisons over consecutive compression expansion cycles were performed using repeated measures ANOVA and comparisons of single values between groups were analyzed using T-test. RESULTS: There were no significant differences between groups in any of the biophysical outcomes of surfactant analysis. The critical function of surfactant, reducing the surface tension to low values upon compression, was similar between healthy dogs and affected drevers. CONCLUSIONS: The etiology of hunting associated pulmonary edema in drever dogs is not due to an underlying surfactant dysfunction.

Successful management of pulmonary edema secondary to accidental electrocution in a young dog.

BACKGROUND: Human records describe pulmonary edema as a life-threatening complication of electric shock. Successful management requires prompt recognition and intensive care. However, in companion animals, electrocutions are rarely reported, even though domestic environments are full of electrical devices and there is always the possibility of accidental injury. Therefore, it is important for veterinarians to know more about this condition in order to achieve successful patient outcomes. CASE PRESENTATION: A 3-month-old male Labrador Retriever was presented with a history of transient loss of consciousness after chewing on a household electrical cord. On admission, the puppy showed an orthopneic position with moderate respiratory distress. Supplemental oxygen via nasal catheter was provided, but the patient showed marked worsening of respiratory status. Point-of-care ultrasound exams suggested neurogenic pulmonary edema due to electrical shock close to the central nervous system and increased B-lines without evidence of cardiac abnormalities. Mechanical ventilation of the patient was initiated using volume-controlled mode with a tidal volume of 9 to 15 ml/kg until reaching an end-tidal carbon dioxide ≤ 40 mm Hg, followed by a stepwise lung-recruitment maneuver in pressure-controlled mode with increases of the peak inspiratory pressure (15 to 20 cm H2O) and positive end-expiratory pressure (3 to 10 cm H2O) for 30 min, and return to volume-controlled mode with a tidal volume of 15 ml/kg until reaching a peripheral oxygen saturation ≥ 96%. Weaning from the ventilator was achieved in six hours, and the patient was discharged two days after admission without neurological or respiratory deficits. CONCLUSIONS: We present a rather unusual case of a neurogenic pulmonary edema subsequent to accidental electrocution in a dog. Timely diagnosis by ultrasound and mechanical ventilation settings are described. Our case highlights that pulmonary edema should be considered a potentially life-threatening complication of electrical shock in small animal emergency and critical care medicine.

Successful treatment of acute respiratory failure following hypertensive crisis in a dog with presumed pheochromocytoma or paraganglioma.

Background: Acute respiratory failure has been reported as one of the manifestations of hypertensive crisis in pheochromocytoma in human medicine. In dogs, no reports have been described as acute respiratory failure following hypertensive crisis. Here, we report the clinical presentation, course, and treatment of acute respiratory failure following the hypertensive crisis in a dog with presumed pheochromocytoma or paraganglioma. Case Description: A 12-year-old neutered male toy poodle was referred for the diagnostic evaluation of a right adrenal gland mass. The dog suddenly exhibited severe dyspnea with abnormal hypertension (systolic blood pressure >200 mmHg) 15 minutes after recovery from the anesthesia for the computed tomography (CT) examination. Pulmonary CT and ultrasonography findings suggested acute onset of severe pulmonary edema. Pulmonary edema was treated with mechanical ventilation (pressure-support ventilation with continuous positive airway pressure) and negative fluid balance after the administration of furosemide. Weaning from mechanical ventilation was successful 24 hours after the onset of respiratory failure. Finally, the dog was discharged 3 days after weaning from ventilation without complications. Conclusion: This report outlines a case of acute respiratory failure following a hypertensive crisis requiring mechanical ventilatory management in a dog. The onset and progression of pulmonary edema were extremely rapid. However, improvement in pulmonary edema was also rapid. Hemodynamic stability, in addition to prompt diagnosis and aggressive therapeutic intervention, including mechanical ventilation, may have contributed to the good prognosis of pulmonary edema following hypertensive crisis in a dog, which we attribute to a catecholamine storm.

Treatment of recurrent hunting-associated respiratory distress episodes in 2 dogs.

Noncardiogenic pulmonary edema (NCPE) in hunting dogs is an uncommon and poorly described condition for which no preventive treatment is available. Two dogs were presented for recurrent respiratory distress strictly associated with hunting activities. Diagnosis was based on bilateral, symmetrical, interstitial-to-alveolar pattern in the caudodorsal lung fields on thoracic radiographs, exclusion of other causes, and spontaneous clinical and radiographic improvement. Considering that the pathogenesis of exercise-induced NCPE likely involves α- and ß-adrenergic overstimulation, treatment with sympathetic blockers was used in both dogs. The first dog no longer showed respiratory signs during hunting activities. However, treatment failed to prevent respiratory distress in the other dog. Based on the large number of red blood cells in the bronchoalveolar lavage fluid of the second dog, exercise-induced pulmonary hemorrhage was suspected, as described in racing horses. The loop diuretic furosemide successfully prevented further hunting-associated respiratory distress episodes in this dog.

Continuous positive airway pressure ventilation in dogs with acute cardiogenic pulmonary edema is associated with improved clinical parameters and reduced diuretic and oxygen requirements.

OBJECTIVE: To retrospectively compare efficacy of a continuous positive airway pressure (CPAP) helmet against standard oxygen supplementation (STD) administered by nasal cannulae in dogs with acute cardiogenic pulmonary edema (ACPE). ANIMALS: 83 dogs (STD group, n = 41; CPAP group, 42) hospitalized for ACPE (January 2019 to April 2021). METHODS: Mean respiratory rate, heart rate, systolic arterial pressure, and rectal body temperature were compared between and within groups before and at 1 (T1), 2 (T2), 3 (T3), 6 (T6), and 12 (T12) hours from the beginning of STD/CPAP therapy. Duration of oxygen supplementation, hospitalization time, total diuretic dose, additional pharmacological interventions and mortality rates were compared between groups. The veterinary bedside lung ultrasound in emergency score, thoracic radiographs, and arterial blood parameters were compared between and within groups before and at the end of CPAP/STD therapy. RESULTS: Within both groups, clinical parameters decreased during the observation period. Mean respiratory rate and heart rate were significantly lower in the CPAP group than the STD group at T1, T2, T3, T6, and T12. Mean systolic arterial pressure was significantly lower in the CPAP group than the STD group at T2, T3, T6, and T12. Mean oxygen supplementation duration, cumulative loop diuretic dose, and both veterinary bedside lung ultrasound in emergency score and arterial PaCO2 at the end of CPAP/STD therapy were significantly lower in the CPAP group than the STD group. No significant differences were observed in hospitalization time and mortality rates. CLINICAL RELEVANCE: The addition of helmet CPAP compared with standard oxygen administration showed a faster clinical improvement with lower cumulative loop diuretic and shorter oxygen supplementation in dogs hospitalized for ACPE.

Echocardiographic caudal vena cava measurements in healthy cats and in cats with congestive heart failure and non-cardiac causes of cavitary effusions.

BACKGROUND: Echocardiographic indices of the inferior vena cava have been associated with elevated right atrial pressures in humans. HYPOTHESIS/OBJECTIVES: Describe caudal vena caval (CVC) sonographic dimensions in healthy cats compared to cats with cardiogenic cavitary effusion (CCE), cardiogenic pulmonary edema (CPE), or non-cardiac causes of cavitary effusion (NCE). ANIMALS: 30 healthy control cats and 52 client-owned cats with CCE, CPE, or NCE examined at two university hospitals. METHODS: Sagittal 2-dimensional (2D) and M-mode CVC dimensions were acquired from the subxiphoid view. Caudal vena cava collapsibility index (CVC-CI) was calculated. Variables were compared between study groups using Kruskal-Wallis and Dunn's Bonferroni testing. Receiver operating characteristic curves were used to assess sensitivity and specificity for diagnostic categories. RESULTS: Healthy cats had sagittal 2D and M-mode (median, interquartile range) CVC maximal dimensions of 2.4 mm (1.3-4.0) and 3.4 mm (1.5-4.9) and CVC-CI of 52% (45.2-61.8) and 55% (47.8-61.3), respectively. The CVC maximal dimensions in healthy controls were smaller than in cats with cavitary effusions or pulmonary edema (all P<0.05). CVC-CI was different between CCE and NCE (P<0.0001) with cutoffs of CVC-CI ≤38% (2D) or ≤29% (M-mode) being 90.5% and 85.7% sensitive, and 94.4% and 100% specific for diagnosis of CCE, respectively. CONCLUSIONS AND CLINICAL IMPORTANCE: Caudal vena cava measurements are larger in cats with cavitary effusions and cats with CPE than healthy cats. In cats with cavitary effusion, decreased CVC-CI, ≤38% (2D) or ≤29% (M-mode), was helpful in distinguishing between cardiogenic and noncardiogenic etiology.

Retrospective evaluation of noncardiogenic pulmonary edema in dogs and cats (2000-2021): 31 cases.

OBJECTIVE: To characterize the clinical features of noncardiogenic pulmonary edema (NCPE), etiology, and outcome in dogs and cats. The study also aimed to evaluate associations with mortality. DESIGN: Retrospective study. SETTING: University teaching hospital. ANIMALS: Thirty dogs and 1 cat, all client owned. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Data collected included animal characteristics, clinical history, evaluation of oxygenation, radiographic features, treatments, and outcomes. Causes of NCPE included upper airway obstruction, electrocution, drowning, neurogenic etiology, and unknown. The etiology was known in 21 of 31 cases (68%), while the etiology of the remaining 10 cases (32%) was classified as unknown. The most common cause for NCPE was upper airway obstruction, found in 14 of 31 cases (45%). The majority of thoracic radiographs showed a mixed interstitial-to-alveolar pulmonary pattern with a diffuse distribution (52%). Oxygen therapy was administered to 27 dogs (90%). Furosemide was administered to 12 dogs (40%). The median duration of hospitalization was 48 hours (range: 1-192). Twenty-three animals (74%) survived to discharge. Six dogs were mechanically ventilated, with only 2 of them (33%) surviving to discharge. The requirement for mechanical ventilation was the only parameter associated with mortality (P = 0.03). CONCLUSIONS: NCPE is a heterogenous disease process that is most common in dogs. There are a variety of causes, but upper airway obstruction appears to be the most common. The overall prognosis is good in animals that do not require mechanical ventilation.

Noncardiogenic pulmonary edema in small animals.

OBJECTIVE: To review various types of noncardiogenic pulmonary edema (NCPE) in cats and dogs. ETIOLOGY: NCPE is an abnormal fluid accumulation in the lung interstitium or alveoli that is not caused by cardiogenic causes or fluid overload. It can be due to changes in vascular permeability, hydrostatic pressure in the pulmonary vasculature, or a combination thereof. Possible causes include inflammatory states within the lung or in remote tissues (acute respiratory distress syndrome [ARDS]), airway obstruction (post-obstructive pulmonary edema), neurologic disease such as head trauma or seizures (neurogenic pulmonary edema), electrocution, after re-expansion of a collapsed lung or after drowning. DIAGNOSIS: Diagnosis of NCPE is generally based on history, physical examination, and diagnostic imaging. Radiographic findings suggestive of NCPE are interstitial to alveolar pulmonary opacities in the absence of signs of left-sided congestive heart failure or fluid overload such as cardiomegaly or congested pulmonary veins. Computed tomography and edema fluid analysis may aid in the diagnosis, while some forms of NCPE require additional findings to reach a diagnosis. THERAPY: The goal of therapy for all types of NCPE is to preserve tissue oxygenation and reduce the work of breathing. This may be achieved by removing the inciting cause (eg, airway obstruction) and cage rest in mild cases and supplemental oxygen in moderate cases and may require mechanical ventilation in severe cases. PROGNOSIS: Prognosis is generally good for most causes of veterinary NCPE except for ARDS, although data are scarce for some etiologies of NCPE.

Role of echocardiographic views adapted for lung evaluation in diagnosis of cardiogenic pulmonary edema in Dogs.

The objective of this study was to determine whether echocardiographic views adapted for lung evaluation may aid in diagnosis of dyspnea in dogs. Fifteen chronic valvular heart disease (CVHD) dogs without cardiac remodeling, 30 CVHD dogs with cardiac remodeling, 15 CVHD dogs with cardiogenic pulmonary edema and 15 dogs with pulmonary disease were prospectively enrolled. Loop recordings of pericardial-lung ultrasound were gathered during echocardiographic evaluation, and four videos of 4 different adapted views were recorded for each dog. Chest X-rays were used as reference-standard for pulmonary edema and/or disease. The videos were classified based on the number of B- lines as NEGATIVE (0, 1, 2 or 3) or POSITIVE (> 3 or confluent). Accuracy of a POSITIVE classification in identifying pulmonary edema and/or disease was calculated. Multivariate analyses were performed using echocardiographic variables that reflect increased left ventricular filling pressure (LVFP) to distinguish pulmonary edema from disease. Results showed that a POSITIVE classification distinguished dogs with pulmonary edema or disease from asymptomatic CVHD dogs in all four views. The best views were right parasternal short axis at papillary muscle level and long axis 4- chamber view, both with the same sensitivity (86.7%) and a specificity of 95.6% and 82.2%, respectively. Multivariate analyses showed that adding cutoff values of peak E wave > 130, E/IVRT > 2.5 or LA/Ao > 2.0 distinguished pulmonary edema from disease with 100% specificity. In conclusion, echocardiographic views adapted for lung evaluation, in addition to conventional echocardiography, may help identify the cause of dyspnea in dogs.

Radiographic features of cardiogenic pulmonary oedema in cats with left-sided cardiac disease: 71 cases.

OBJECTIVES: The aims of this study were to describe the radiographic features of cardiogenic pulmonary oedema (CPE) in a large group of cats with left-sided cardiac disease, and to determine the association between the radiographic features of CPE and the underlying cardiac disease. METHODS: Thoracic radiographs of cats with CPE and echocardiographic evidence of left-sided cardiac disease and left atrial enlargement (LAE) were reviewed, and cardiac silhouette, pulmonary vessels and pulmonary parenchyma evaluation were performed. Interstitial and/or alveolar patterns were classified according to their distribution (ie, diffuse, multifocal or focal) and location (ie, craniodorsal, cranioventral, caudodorsal, caudoventral and perihilar). A Student's t-test and Mann-Whitney U-test, or the two-proportion z-test, were used to compare continuous or categorical variables, respectively, between cats affected by the two most represented cardiac diseases, namely hypertrophic cardiomyopathy (HCM) and restrictive cardiomyopathy (RCM). RESULTS: Seventy-one cats were included; among them, 46 (64.7%) and 13 (18.3%) had presented for HCM and RCM, respectively. Subjective and objective cardiomegaly, and subjective and objective LAE were detected in 97.2% and 91.9% of cats and in 80.3% and 40.6% of cats, respectively. Pulmonary artery abnormalities, in particular caudal pulmonary artery dilation, were found in 77.5% of cats. Pulmonary artery to pulmonary vein ratio = 1 was found in 71.8% and 55% cats on right lateral and ventrodorsal or dorsoventral views, respectively. Interstitial (57.8%) and mixed interstitial-alveolar (38%) pattern, multifocal (84.5%) and symmetrical (75%) distribution with prevalent ventrocaudal (65.6% of cats) and ventrocranial (60.9% of cats) locations were most frequently observed. No difference was found for any of these radiographic features between cats with HCM and RCM. CONCLUSIONS AND RELEVANCE: Moderate-to-severe cardiomegaly and LAE, caudal pulmonary artery and vein dilation, as well as a ventral, multifocal and symmetrical interstitial pulmonary pattern, were the main radiographic features of CPE in evaluated cats. Underlying cardiac disease did not influence the aforementioned radiographic features.

Retrospective evaluation of clinical signs, clinical course, and prognosis between dogs with left atrial rupture secondary to myxomatous mitral valve disease and those with neoplastic cardiac tamponade (2015-2019): 70 cases.

OBJECTIVE: To describe the clinical signs, clinical course, and prognosis of suspected left atrial rupture (LAR) secondary to myxomatous mitral valve disease (MMVD) in dogs and to compare them with dogs with suspected neoplastic cardiac tamponade (NCT). DESIGN: Retrospective study from November 2015 to October 2019 SETTING: An out-of-hours Emergency Animal Hospital. ANIMALS: Twenty-three dogs with LAR secondary to MMVD (LAR group) and 47 dogs with NCT (NCT group). INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The following were the characteristics of the study population (LAR group vs NCT groups) with P < 0.05 as the significance threshold: male sex, 83% vs 66%; median age, 11.9 vs 12.5 years; and median weight, 3.8 vs 6.4 kg (P < 0.001). Chihuahuas and Miniature Dachshunds were overrepresented in the LAR and NCT groups, respectively. Statistically different clinical findings between the 2 groups were as follows (LAR vs NCT): pulmonary edema, 43% vs 0%; pericardial thrombus, 70% vs 6% (P < 0.001); ineffectiveness of pericardiocentesis (whether aspiration of pericardial fluid was successful or not), 58% vs 2% (P < 0.001); mortality rate within 48 hours of visiting hospital, 35% vs 9% (P < 0.01). No significant difference was observed in survival time after discharge between the 2 groups. CONCLUSIONS: The proportion of dogs with a diagnosis of LAR secondary to MMVD in dogs with cardiac tamponade was higher than the previously reported rate. Furthermore, the frequency of pulmonary edema, ineffectiveness of pericardiocentesis, and short-term mortality rate was higher in the LAR group than in the NCT group.

Reduced risk of arterial thromboembolism in cats with pleural effusion due to congestive heart failure.

OBJECTIVES: The aim of the study was to determine whether cardiogenic pleural effusion in cats is associated with a lower risk of arterial thromboembolism (ATE) compared with cats with cardiac disease without evidence of pleural effusion. METHODS: A cross-sectional study was conducted on owned cats with natural occurring cardiac diseases. Cats included were classified in three groups: those with cardiac disease but no evidence of congestive heart failure (CHF); those with evidence of cardiogenic pulmonary oedema; and those with evidence of cardiogenic pleural effusion. Prevalence of ATE was calculated and the variables analysed for an association with this outcome were the presence and type of CHF, sex and neuter status, age, breed, type of cardiac diseases and left atrial (LA) dimension. A multivariable logistic regression model was used to fit the association between ATE and these variables. RESULTS: A total of 366 cats with cardiac disease met the inclusion criteria: 179 were included in the group with cardiac disease but no evidence of CHF, 66 in the group with evidence of cardiogenic pulmonary oedema and 121 in the group with evidence of cardiogenic pleural effusion. Prevalence of ATE (58/366 [15.8%]) was significantly different among groups (with no evidence of CHF, 28/179 [15.6%]; with evidence of cardiogenic pulmonary oedema, 22/66 [33.3%]; with evidence of cardiogenic pleural effusion, 8/121 [6.6%]; P <0.001). Cats with ATE had a significantly higher LA to aortic root ratio (2.30 ± 0.46) than those without ATE (2.04 ± 0.46; P <0.001). Multivariable logistic regression analysis indicated that the group with evidence of cardiogenic pleural effusion was associated with a lower risk of developing ATE compared with groups with cardiac disease but no evidence of CHF and with evidence of cardiogenic pulmonary oedema (P = 0.005 and P <0.001, respectively). CONCLUSIONS AND RELEVANCE: Presence of cardiogenic pleural effusion is associated with a lower risk of developing ATE, while LA enlargement is a risk factor for ATE.

Influence of concurrent lower respiratory tract disease on point-of-care lung ultrasound in small-breed dogs with myxomatous mitral valve disease.

BACKGROUND: Small-breed dogs commonly have concurrent myxomatous mitral valve disease (MMVD) and lower respiratory tract disease (LRTD). HYPOTHESIS: Small-breed dogs with preclinical MMVD and concurrent LRTD have more B-lines on point-of-care lung ultrasound (POC-LUS) compared to dogs without concurrent LRTD and are prone to misdiagnose as cardiogenic pulmonary edema (CPE). ANIMALS: A total of 114 small-breed dogs with preclinical MMVD. METHODS: A prospective study was conducted, in which POC-LUS was obtained and the number of B-lines was calculated by a single clinician using the Veterinary Bedside Lung Ultrasound Examination protocol. The presence/absence of LRTD was assessed by clinicians blinded to the POC-LUS results. RESULTS: Fifty and 64 dogs were in ACVIM stage B1 and B2, respectively. The presence of LRTD was prevalent in 74.6% (85/114) of small-breed dogs with preclinical MMVD. When a previously reported criterion for CPE diagnosis (≥2 sites with >3 B-lines/site) was applied, false-positive results were observed in 15.8% (18/114) of dogs with preclinical MMVD. The summated number of B-lines (3 vs. 1, P = .003), as well as the false-positive rate (20% vs 3%, P = .04), were significantly higher in dogs with LRTD compared with dogs without LRTD. Multivariable logistic regression showed the presence of abnormalities other than B-line on POC-LUS (eg, thickened pleura or consolidation) could predict false-positive results (odds ratio = 3.75, 95% confidence intervals 1.12-12.54; P = .03) after adjustment for other clinical and echocardiographic factors. CONCLUSIONS AND CLINICAL IMPORTANCE: Concurrent LRTD and abnormalities other than B-lines should be considered in the interpretation of POC-LUS in MMVD dogs.

Comparison of artificial intelligence to the veterinary radiologist's diagnosis of canine cardiogenic pulmonary edema.

Application of artificial intelligence (AI) to improve clinical diagnosis is a burgeoning field in human and veterinary medicine. The objective of this prospective, diagnostic accuracy study was to determine the accuracy, sensitivity, and specificity of an AI-based software for diagnosing canine cardiogenic pulmonary edema from thoracic radiographs, using an American College of Veterinary Radiology-certified veterinary radiologist's interpretation as the reference standard. Five hundred consecutive canine thoracic radiographs made after-hours by a veterinary Emergency Department were retrieved. A total of 481 of 500 cases were technically analyzable. Based on the radiologist's assessment, 46 (10.4%) of these 481 dogs were diagnosed with cardiogenic pulmonary edema (CPE+). Of these cases, the AI software designated 42 of 46 as CPE+ and four of 46 as cardiogenic pulmonary edema negative (CPE-). Accuracy, sensitivity, and specificity of the AI-based software compared to radiologist diagnosis were 92.3%, 91.3%, and 92.4%, respectively (positive predictive value, 56%; negative predictive value, 99%). Findings supported using AI software screening for thoracic radiographs of dogs with suspected cardiogenic pulmonary edema to assist with short-term decision-making when a radiologist is unavailable.

Non-cardiogenic pulmonary oedema complicating balloon valvuloplasty and stent angioplasty of severe pulmonary valve stenosis in four dogs.

In dogs, balloon valvuloplasty is considered the treatment of choice for severe pulmonary valve stenosis, and this technique is currently performed routinely in specialist referral practices with low morbidity and mortality. Stent angioplasty has also been recently proposed as a viable treatment option. The present case series describes the clinical course of four dogs with severe pulmonary valve stenosis, treated with balloon valvuloplasty or stent angioplasty at four different institutions, which developed non-cardiogenic pulmonary oedema perioperatively after apparently successful dilation of the pulmonary valve. In three cases, there was evidence of some degree of pulmonary hypertension before ballooning. Despite intensive care, the complication proved fatal in three cases. Clinicians should therefore be aware of this life-threatening complication, previously undescribed in dogs.

Acute pulmonary edema in a dog with severe pulmonary valve stenosis: A rare complication after balloon valvuloplasty.

Pulmonic stenosis is a frequent congenital heart disease in dogs, and the treatment of choice is balloon valvuloplasty which is usually safe and successful. The authors describe for the first time a severe complication after balloon valvuloplasty in a five-month-old dog. After effective treatment, with a considerable drop in right ventricular pressures, the dog developed hypoxemia and dyspnea due to pulmonary edema. The dog underwent intensive care and symptoms improved after a few hours of oxygen therapy, continuous positive airway pressure, and furosemide. Although this event is rare, it could have a large impact on patient survival and should be considered in the treatment of severe pulmonary valve stenosis in the future.

Retrospective evaluation of negative-pressure pulmonary edema in dogs (2006-2018): 35 cases.

OBJECTIVE: To describe the clinical characteristics and outcomes in a population of dogs with negative-pressure pulmonary edema (NPPE) and to identify the main causes of the disease. To evaluate any associations with morbidity and mortality. DESIGN: Retrospective study. SETTING: Three university teaching hospitals and 2 private referral centers in the United Kingdom. ANIMALS: Thirty-five client-owned dogs presented with NPPE. INTERVENTIONS: None MEASUREMENTS AND MAIN RESULTS: Data collected included patient characteristics, clinical history, clinicopathological abnormalities, radiographic features, treatments, and outcomes. The median age was 4 months (range 2-90) and median weight was 7.1 kg (range 1.7-37.2). There were many causes of NPPE including leash tugs, near hanging, accidental choking, anatomical obstruction to airflow, and purposeful airway obstruction by people. The most common cause of NPPE was accidental choking (40% of cases). Dogs with an anatomical obstruction were older than 24 months. Hypoxemia with an increased alveolar-arterial gradient was common on presentation. The majority of thoracic radiographs (65.7%) showed an alveolar or interstitial pattern in the caudodorsal area as previously described in the literature. Oxygen therapy was administered to 33 (94.3%) dogs. Furosemide was administered to 18 (51.4%) dogs. The median length of hospitalization was 2 days (range 0-14). Twenty-eight (80%) dogs survived to discharge. Seven dogs were mechanically ventilated and only 2 of them (28.6%) survived to discharge. The requirement for mechanical ventilation was the only parameter associated with mortality (P < 0.001). CONCLUSIONS: Most cases of NPPE occur in juvenile dogs. Different incidents associated with upper airway obstruction can produce an episode of NPPE. Choking on food or toys and near hanging have not been previously described in the veterinary literature as inciting causes of NPPE. The overall prognosis is good.

Application of α2 -adrenergic agonists combined with anesthetics and their implication in pulmonary intravascular macrophages-insulted pulmonary edema and hypoxemia in ruminants.

Alpha2 -adrenergic agonists have been implicated in the development of pulmonary edema (PE) and sustained hypoxemia that lead to life-threatening pulmonary distress in ruminants, especially with sensitive and compromised animals. Recently, there is limited understanding of exact mechanism underlying pulmonary alterations associated with α2 -adrenergic agonist administration. Ruminants have a rich population of pulmonary intravascular macrophages (PIMs) in the pulmonary circulation, which may be involved in the development of pulmonary alveolo-capillary barrier damage. Hence, the central thesis of this review is overviewing the literatures regarding the systemic use of α2 -adrenergic agonists in domestic ruminants, focusing on their pulmonary side effects, especially on the influence of PIMs on the lung. At this moment, further studies are needed to provide a clear emphasis and better understanding of the potential role of PIMs in the lung pathophysiology associated with α2 -adrenergic agonists. These preliminary studies would be potentially to develop future medications and intervention targets that may be helpful to alleviate or prevent the critical striking pulmonary effects, and thereby improving the safety of α2 -agonist application in ruminants.

A case of a complete atrioventricular canal defect in a ferret.

BACKGROUND: Atrioventricular canal defect is a rare congenital disorder of the heart and describes the presence of an atrial septal defect, a variable presentation of ventricular septal alterations including ventricular septal defect malformations in the mitral and tricuspid valves. The defect has been described in human beings, dogs, cats, pigs, and horses. CASE PRESENTATION: This paper describes the case of a complete atrioventricular canal defect in a four-year-old intact male pet ferret (Mustela putorius furo), which was presented due to posterior weakness, ataxia, and decreased appetite. A loud systolic murmur, dyspnea, and hind limb paraparesis were detected during the clinical examination. Thoracic radiographs showed generalized cardiomegaly and lung edema. ECG showed sinus rhythm with prolonged P waves and QRS complexes. Echocardiography showed a large atrial septal defect, atrioventricular dysplasia, and a ventricular septal defect. Palliative treatment with oxygen, furosemide, spironolactone, enalapril, diltiazem, and supportive care was chosen as the therapy of choice. The ferret recovered gradually during hospitalization. A follow-up examination at three and six months showed stabilization of cardiac function. CONCLUSIONS: To the authors knowledge, this is the first time an atrioventricular canal defect has been described in a pet ferret.

Utility of point-of-care lung ultrasound for monitoring cardiogenic pulmonary edema in dogs.

BACKGROUND: Point-of-care lung ultrasound (LUS) is an effective tool to diagnose left-sided congestive heart failure (L-CHF) in dogs via detection of ultrasound artifacts (B-lines) caused by increased lung water. HYPOTHESIS/OBJECTIVES: To determine whether LUS can be used to monitor resolution of cardiogenic pulmonary edema in dogs, and to compare LUS to other indicators of L-CHF control. ANIMALS: Twenty-five client-owned dogs hospitalized for treatment of first-onset L-CHF. METHODS: Protocolized LUS, thoracic radiographs (TXR), and plasma N-terminal pro-B-type natriuretic peptide were performed at hospital admission, hospital discharge, and recheck examinations. Lung ultrasound findings were compared between timepoints and to other clinical measures of L-CHF. RESULTS: From time of hospital admission to discharge (mean 19.6 hours), median number of LUS sites strongly positive for B-lines (>3 B-lines per site) decreased from 5 (range, 1-8) to 1 (range, 0-5; P < .001), and median total B-line score decreased from 37 (range, 6-74) to 5 (range, 0-32; P = .002). Lung ultrasound indices remained improved at first recheck (P < .001). Number of strong positive sites correlated positively with respiratory rate (r = 0.52, P = .008) and TXR edema score (r = 0.51, P = .009) at hospital admission. Patterns of edema resolution differed between LUS and TXR, with cranial quadrants showing more significant reduction in B-lines compared to TXR edema score (80% vs 29% reduction, respectively; P = .003). CONCLUSIONS AND CLINICAL IMPORTANCE: Lung ultrasound could be a useful tool for monitoring resolution of pulmonary edema in dogs with L-CHF.