TRANSTHORACIC LUNG ULTRASOUND IN NORMAL DOGS AND DOGS WITH CARDIOGENIC PULMONARY EDEMA: A PILOT STUDY

Pulmonary edema is the most common complication of left‐sided heart failure in dogs and early detection is important for effective clinical management. In people, pulmonary edema is commonly diagnosed based on transthoracic ultrasonography and detection of B line artifacts (vertical, narrow‐based, well‐defined hyperechoic rays arising from the pleural surface). The purpose of this study was to determine whether B line artifacts could also be useful diagnostic predictors for cardiogenic pulmonary edema in dogs. Thirty‐one normal dogs and nine dogs with cardiogenic pulmonary edema were prospectively recruited. For each dog, presence or absence of cardiogenic pulmonary edema was based on physical examination, heartworm testing, thoracic radiographs, and echocardiography. A single observer performed transthoracic ultrasonography in all dogs and recorded video clips and still images for each of four quadrants in each hemithorax. Distribution, sonographic characteristics, and number of B lines per thoracic quadrant were determined and compared between groups. B lines were detected in 31% of normal dogs (mean 0.9 ± 0.3 SD per dog) and 100% of dogs with cardiogenic pulmonary edema (mean 6.2 ± 3.8 SD per dog). Artifacts were more numerous and widely distributed in dogs with congestive heart failure (P < 0.0001). In severe cases, B lines increased in number and became confluent. The locations of B line artifacts appeared consistent with locations of edema on radiographs. Findings from the current study supported the use of thoracic ultrasonography and detection of B lines as techniques for diagnosing cardiogenic pulmonary edema in dogs.     

Negative Pressure Pulmonary Edema as a Post-Anesthetic Complication Associated With Upper Airway Obstruction in a Horse

An 8-year-old Trakehner mare developed fulminant pulmonary edema following suspected upper airway obstruction 50 minutes into an otherwise unremarkable anesthetic recovery after surgery for left cricoarytenoideus dorsalis muscle reinnervation and ventriculocordectomy. Establishing a patent airway by orotracheal reintubation and cardiopulmonary resuscitation attempts were unsuccessful. Gross, histological, and electron microscopic postmortem examination showed severe hemorrhagic pulmonary edema. Laryngeal swelling or hemorrhage were not evident, suggesting laryngospasm or functional airway collapse associated with the underlying left laryngeal paralysis, as a cause of the upper airway obstruction. Negative pressure pulmonary edema is rarely reported in the veterinary literature as a postanesthetic complication.     

RADIOGRAPHIC APPEARANCE OF PRESUMED NONCARDIOGENIC PULMONARY EDEMA AND CORRELATION WITH THE UNDERLYING CAUSE IN DOGS AND CATS

Noncardiogenic pulmonary edema is an important cause of respiratory disease in dogs and cats but few reports describe its radiographic appearance. The purpose of this retrospective case series study was to describe radiographic findings in a large cohort of dogs and cats with presumed noncardiogenic pulmonary edema and to test associations among radiographic findings versus cause of edema. Medical records were retrieved for dogs and cats with presumed noncardiogenic edema based on history, radiographic findings, and outcome. Radiographs were reviewed to assess lung pattern and distribution of the edema. Correlation with the cause of noncardiogenic pulmonary edema was evaluated with a Fisher's exact test. A total of 49 dogs and 11 cats were included. Causes for the noncardiogenic edema were airway obstruction (n = 23), direct pulmonary injury (n = 13), severe neurologic stimulation (n = 12), systemic disease (n = 6), near‐drowning (n = 3), anaphylaxis (n = 2) and blood transfusion (n = 1). Mixed, symmetric, peripheral, multifocal, bilateral, and dorsal lung patterns were observed in 44 (73.3%), 46 (76.7%), 55 (91.7%), 46 (76.7%), 46 (76.7%), and 34 (57.6%) of 60 animals, respectively. When the distribution was unilateral, pulmonary infiltration involved mainly the right lung lobes (12 of 14, 85.7%). Increased pulmonary opacity was more often asymmetric, unilateral, and dorsal for postobstructive pulmonary edema compared to other types of noncardiogenic pulmonary edema, but no other significant correlations could be identified. In conclusion, noncardiogenic pulmonary edema may present with a quite variable radiographic appearance in dogs and cats.     

Pulmonary edema in a dog with acute pancreatitis and cardiac disease

Acute pancreatitis and cardiac disease were diagnosed in a dog with pulmonary edema. The early clinical course and initial thoracic radiographs suggested that the pulmonary edema was noncardiogenic. The late clinical course was complicated by heart failure. The dog died, and a necropsy was performed. Histologically, an acute, severe capillary-alveolar membrane lesion was found in the lungs. Review of the human medical literature indicated that respiratory complications, including pulmonary edema, are commonly recognized in people with acute pancreatitis. Furthermore, in acute pancreatitis of human beings, the existence of specific mechanisms of pulmonary injury is suspected. Retrospective consideration of this case suggested that the initial pulmonary edema was induced by acute pancreatitis.     

S-亚硝基谷胱甘肽对实验性心源性肺水肿的防治作用

对小鼠腹腔注射肾上腺素造成实验性心源性肺水肿动物模型,观察S-亚硝基谷胱甘肽（GSNO）对肺水肿的防治作用。结果显示,与阳性对照相比,GSNO预防组和治疗组小鼠存活率极显著提高（P〈0.01）,肺指数极显著降低（P〈0.01）,肺组织的病理变化也明显减轻。提示：GSNO对心源性肺水肿具有明显的预防和治疗作用。     

Post‐anesthetic pulmonary edema in two horses

Case 1 A two‐year old, 462 kg Standard bred horse was anesthetized for arthroscopy and castration. During anesthesia, hyperemia of the mucosal membranes and urticaria were noticed. During 5 hours of anesthesia subcutaneous edema of the eyelids and neck region developed. In the recovery box, the orotracheal (OT) tube was left in situ and secured in place with tape. Following initial attempts to stand, the horse became highly agitated and signs consistent with pulmonary edema developed subsequently. Arterial hypoxemia (PaO₂: 3.7 kPa [28 mmHg]) and hypocapnia (PaCO₂: 3.1 kPa [23 mmHg]) were confirmed. Oxygen and furosemide were administered. The horse was assisted to standing with a sling. Therapy continued with bilateral intra‐nasal oxygen insufflation. Ancillary medical therapy included flunixin meglumine, penicillin, gentamycin and dimethylsulfoxide. Following 7 hours of treatment the arterial oxygen tensions began to increase towards normal values. Case 2 An 11‐year old, 528 kg Paint horse was anesthetized for surgery of a submandibular mass. The 4‐hour anesthetic period was unremarkable. The OT tube was left in situ for the recovery. During recovery, the horse was slightly agitated and stood after three attempts. Clinical signs consistent with pulmonary edema and arterial hypoxemia (PaO₂: 5 kPa [37.5 mmHg]) subsequently developed following extubation. Respiratory signs resolved with medical therapy, including unilateral nasal oxygen insufflation, furosemide, flunixin meglumine and dimethylsulfoxide. The diagnosis of pulmonary edema in these horses was made by clinical signs and arterial blood‐gas analysis. While pulmonary radiographs were not taken to confirm the diagnosis, the clinical signs following anesthesia support the diagnosis in both cases. The etiology of pulmonary edema was most likely multifactorial.     

Suspected toxicosis after topical administration of minoxidil in 2 cats

Objective: To discuss the clinical presentation and necropsy findings of 2 cats after topical administration of a minoxidil solution. Additionally, a potential management plan is offered for future cases. Case summary: Two cats with dermal exposure to topical minoxidil solution were identified from the ASPCA Animal Poison Control Center (APCC) files. Both cats were presented with lethargy and dyspnea within 36 hours of exposure. The cats were hypothermic, and had pulmonary edema and pleural effusion present on thoracic radiography. Both cats died despite supportive care. Necropsy of both cats confirmed pleural effusion and pulmonary edema and indicated cardiac compromise. New or unique information provided: Topical administration of minoxidil solution may cause life‐threatening pulmonary edema, pleural effusion, and cardiac dysfunction in the cat.     

Pulmonary edema and emphysema in cattle after intraruminal and intravenous administration of 3-methylindole.

Intraruminal and intravenous administration of 3-methylindole (3MI; skatole) caused interstitial pulmonary edema and emphysema in cattle. In 3 adult heifers given the intraruminal dose of 0.2 g of 3 MI per kilogram of body weight, clinical signs of respiratory disease appeared between 6 and 12 hours after dosing, and death due to pulmonary edema and emphysema occurred at 33, 69, and 72 hours. The mean plasma concentration of 3MI became maximal (18.5 mug/ml) at 3 hours and then decreased to low concentrations by 48 hours. In 2 heifers given an intraruminal dose of 0.1 g of 3MI/kg, clinical signs developed, but they did not die during the 96-hour experiment. The mean plasma concentration of 3 MI became maximal (16.8 mug/ml) at 3 hours and decreased to 1.6 and 0.4 mug/ml at 12 and 36 hours, respectively. At necropsy of the heifers, the lung were large, firm, dark red, and heavier than normal. Diffuse pulmonary edema was the predominant change in cattle which died early, and interstitial emphysema was more severe at later stages of the disease. During the early stages, alveoli were overdistended, and a few more ruptured. Most alveolar spaces were filled with proteinaceous residue, but the alveolar septums were smooth and of normal thickness. At later stages, proliferation of alveolar cells was observed, and alveolar septums were thickened. In 3 cows given 0.06 g of 3MI/kg by jugular infusion, clinical signs appeared in all cows, and 1 cow died of pulmonary edema and emphysema 56 hours after the infusion was started. Severe pulmonary lesions seen in all of the cows given a 3MI infusion were similar to those in the cows given an intraruminal dose of 3MI. The mean plasma concentration of 3MI increased to 10.7 mug/ml at 9 hours after starting the infusion and decreased to 0.5 mug/ml at 18 hours. The results indicate that 3MI, a product of ruminal tryptophan fermentation, can cause pulmonary edema and interstitial emphysema in cattle and support the hypothesis that 3MI is the causative agent in tryptophan-induced pulmonary disease.     

Characterization of an epizootic of pulmonary edema in swine associated with fumonisin in corn screenings.

In 1989, corn screenings were associated with acute interstitial pulmonary edema, hydrothorax, and death in swine. Attack rate was 5-50%, case fatality rate was 50-90%, and clinical course was 1-2 days. Screenings from farms with pigs affected with pulmonary edema contained 20-330 micrograms fumonisin B1 per gram. Screenings containing 92 micrograms fumonisin B1 per gram fed to weanling pigs caused pulmonary edema and death. Sterilized corn inoculated with Fusarium moniliforme and diluted 1:1 with clean corn contained fumonisin B1 (17 micrograms/g) and caused acute pulmonary edema when fed for 5 days. Survivors developed subacute hepatotoxicosis with individual hepatocellular necrosis, hepatomegalocytosis, and increased numbers of mitotic figures. Similar liver lesions occurred in pigs given fumonisin B1 intravenously at 0.8 mg/kg body weight for 14 days.     

Suspected air embolism associated with post-anesthetic pulmonary edema and neurologic sequelae in a horse

A 523 kg Quarter Horse was anesthetized for unilateral eye enucleation. The anesthetic period was unremarkable. During anesthetic recovery the cap on the jugular venous catheter became dislodged. Clinical signs of pulmonary edema associated with moderate arterial hypoxemia subsequently developed. Although pulmonary edema resolved with medical therapy, the day following anesthetic recovery, clinical signs of vestibular disease and blindness developed. Treatment included nasal oxygen insufflation, flunixin meglumine, furosemide, dexamethasone, thiamine, dimethylsulfoxide, antimicrobials, and phenylbutazone. The horse recovered and was discharged from the hospital after 7 days of treatment and was neurologically normal at 6 weeks. While venous air embolism was not confirmed in this case, the catheter cap complication followed by signs of pulmonary edema and neurologic sequelae support the presumptive pathogenesis of this horse's complications. Diagnostic confirmation of air embolism in horses with compatible acute clinical signs should be documented with echocardiography.     

Diagnosis and treatment of presumptive postobstructive pulmonary edema in a Florida panther (Puma concolor coryi).

A free-ranging, adult male Florida panther (Puma concolor coryi) was immobilized and evaluated for hematuria following routine capture. Prior to anesthetic recovery, the panther was fitted with a telemetry collar. After an initially quiet recovery, the panther began thrashing in the transport cage, and was again immobilized. Pink foam was evident from the nostrils, and crackles were ausculted over the chest, indicating pulmonary edema. Postobstructive pulmonary edema was diagnosed based on history, clinical signs, radiographic evaluation, and blood gas analysis. The animal was treated intensively for several hours with diuretics, oxygen, and manual ventilation. The panther responded rapidly to therapy and was released back into the wild 48 hr after presentation. Postobstructive pulmonary edema, also called negative-pressure pulmonary edema, may be underrecognized in veterinary medicine. In this case, the telemetry collar, in conjunction with anesthetic recovery in a small transport crate, may have contributed to tracheal obstruction. Wildlife veterinarians and biologists should be aware of the risk of airway obstruction when placing tracking collars, and animals should be continuously monitored during anesthetic recovery to ensure the presence of a patent airway.     

白苏提取物的毒性研究

瘤胃分别注射白苏挥发油及水煎液，观察中毒山羊的临床病理特征，研究白苏提取物的毒性。结果表明，瘤胃注射20mL白苏挥发油（相当于4．167kg新鲜白苏茎叶），山羊出现明显的中毒反应；而瘤胃注射500mL白苏水煎液（相当于5kg新鲜白苏茎叶）对其无影响。中毒山羊的心、肺血流量先上升后下降，主要临床病理特征为：颈静脉怒张，胸腔积液，心脏扩张、心壁变薄、心肌有出血点，肺水肿，支气管、细支气管内有大量的泡沫。试验进一步证实，白苏挥发油是动物白苏中毒的主要致病因子，其病理演变过程为急性心衰，导致肺水肿。     

Acute pulmonary Sarcocystis falcatula-like infection in three Victoria crowned pigeons (Goura victoria) housed indoors.

Three free-roaming Victoria crowned pigeons (Goura victoria) housed in a completely enclosed tropical exhibit were found dead without antemortem signs of illness. The birds died within 9 days of each other. Gross necropsy revealed moderate pulmonary edema in all three birds. Histopathologic examination revealed pulmonary edema and pulmonary protozoal merozoites compatible with Sarcocystis spp., Toxoplasma gondii, or Neospora spp. infection. Immunohistochemical staining for T. gondii and Neospora spp. were negative. Immunohistochemical staining identified a Sarcocystis falcatula-like parasite in all three birds. It is suspected that new exhibit soil contaminated with feces from the Virginia opossum (Didelphis virginiana) was the source of the infective sporocysts.     

Mycotoxicosis produced in swine by cultural products of an isolate of Aspergillus ochraceus. I. Clinical observations and pathology.

Pigs fed a ration, 25% of which was rice culture, of Aspergillus ochraceus lost weight or failed to gain and became depressed. Some pigs died and most developed subcutaneous edema, hydrothorax, hydroperitoneum, pulmonary atelectasis, edema of the mesentery and perirenal edema. Microscopic lesions in addition to edema were primarily renal and consisted of tubular degeneration and necrosis, hyaline tubular casts, interstitial fibrosis and tubular cell regeneration. The first change found after 3 days was cytoplasmic vacuolation of the convoluted and straight segments of the proximal tubules. Necrotic proximal tubules were found after 4 days and after 9 days degeneration and necrosis involved predominantly proximal tubular segments. Pigs fed a ration, 12.5% of which was rice culture, for 8 weeks did not develop perirenal edema but had firm kidneys. Extensive interstitial fibrosis of the cortical labyrinth was the principal change. Within the fibrous connective tissue, some tubules were necrotic and others were atrophied.     

Postanesthetic Pulmonary Edema In an Arab Stallion

A six-year-old arabian stallion was admitted to The Ohio State University Veterinary Hospital for evaluation and repair of a comminuted fracture of the second phalanx. The horse developed impaired arterial oxygenation during surgey and pulmonary edema post-operatively. We postulate that impaired arterial oxygenation resulted from atelectasis of the dependent lung during annesthesia, and the pulmonary edema occurred following re-expansion of the atelectatic of the initiating cause of the edema, removal of excess lung water from the alveoli, and restoration of normal arterial oxygenation. The horse was fully recovered within 12 hours of initiation of clinical signs of respiratory compromise. The horse was fully recovered within 12 hours of initiation of clinical signs of respiratory compromise. This report describes re-expansion pulmonary edema due to reperfusion injury in a horse, treatment of the condition, and a possible explanation of the pathogenesis of this pulmonary pathology.     

The role of Dirofilaria immitis antigen in the pathogenesis of pulmonary arteritis in the dog. 1. The effects of antigen infusion

The aim of this study was to investigate the correlation between the Dirofilaria immitis antigen and morphology response of pulmonary tissue. The pulmonary arteries of D. immitis naive dogs were infused with an antigenic extract of adult female D. immitis worms. Light and electron microscopy and an assessment of vascular permeability were performed to compare arterial pathology 1 h and 5 days after antigen infusion. Thrombus formation accompanied by perivascular edema was present initially, but it was not detectable after 5 days.     

Blind omphalitis and palatine abscess in a bull calf

Neurological, respiratory, and gastrointestinal signs in a 2-month-old veal calf were suggestive of a possible herd problem. Autopsy revealed an umbilical abscess, an abscess on the soft palate, and mild chronic enteritis and pulmonary edema. Virologic and bacteriologic investigations did not provide a definitive diagnosis.     

一例泰迪犬冠状病毒感染伴发急性肺水肿的病理诊断报告

某宠物主人送检1只4月龄泰迪犬,初步确诊为冠状病毒感染,于输液过程中突然死亡。剖检可见整个肺脏呈深红色,肺叶边缘呈粉红色,切面深红色,支气管断端有大量红色液体渗出;剖开气管可见其浆膜面呈暗红色,腔内充满红色清亮液体;心脏左右心室扩张,质地柔软,心尖钝圆,呈心力衰竭心。对各个脏器取材进行病理组织学观察,主要病变表现为肺脏弥漫性淤血、水肿,心肌纤维局部溶解坏死。诊断该犬因感染冠状病毒后初次洗澡应激加重病情,并且随着大量静脉输液导致或加剧急性肺水肿发生,最终造成该犬急性死亡。对该病例进行了系统地病理剖检和组织病理学观察,为犬科动物和其他动物发生类似病症提供一定的参考。     

Orthodromic Reciprocating Tachycardia and Heart Failure in a Dog With a Concealed Posteroseptal Accessory Pathway

A 4-month-old male Labrador Retriever was presented for recurrent bouts of pulmonary edema associated with tachycardia. Initial physical examination and echocardiography were unremarkable, and the electrocardiogram revealed only an intraventricular conduction disturbance. Subsequent recordings showed paroxysmal supraventricular tachycardia (SVT) (340 beats/min), which consistently produced pulmonary edema. The supraventricular tachycardia was unresponsive to adenosine, esmolol, and propranolol; was variably and transiently responsive to various vagal maneuvers and precordial thumps; and was always responsive to IV diltiazem. Multiple life-threatening episodes of SVT occurred, however, despite the chronic administration of oral diltiazem, propranolol, and procainamide. Diastolic cardiac dysfunction was documented by Doppler echocardiography and was thought to contribute to the development of pulmonary edema. A subsequent electrophysiologic study confirmed the presence of an atrioventricular posteroseptal accessory pathway that participated in orthodromic reciprocating tachycardia. This pathway was determined to conduct only in the retrograde direction ("concealed accessory pathway"). Intraoperative IV procainamide titration terminated the arrhythmia, which could not be reinduced when procainamide blood concentration approximated 20 μg/dL. Increasing the oral procainamide dose to achieve such plasma concentrations was successful in eliminating orthodromic reciprocating tachycardia, preventing heart failure, and returning Doppler indices of diastolic function to normal.