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.     

Acute pulmonary edema after diazepam-ketamine in a dog

An 8-year-old mixed-breed dog was anesthetized for colonoscopy. Moderate sedation was produced by premedication with glycopyrrolate, acepromazine, and hydromorphone, and anesthesia was induced by IV injection of diazepam and ketamine. Frothy, reddish-colored fluid flowed from the endotracheal tube immediately after endotracheal intubation but ceased after several minutes. Furosemide was injected IV. Anesthesia was maintained by sevoflurane in oxygen. Ventilation and arterial blood pressure were satisfactory, however, after oxygen was administered to maintain normal hemoglobin saturation. Radiography revealed changes consistent with a diagnosis of pulmonary edema. The following day, ventricular premature contractions developed and atrial dissociation, valvular regurgitation, and pulmonary hypertension were diagnosed on echocardiography. The proposed etiology is either profound transient hypotension and/or pulmonary hypertension induced by ketamine. The cardiac abnormalities that were present the following day suggest that myocardial dysfunction after induction of anesthesia was more severe than was apparent as assessed by routine physical examination and monitoring methods.     

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.     

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。     

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.     

基于网络药理学探讨麻黄甘草汤治疗肺水肿的作用机制

【目的】预测麻黄甘草汤治疗肺水肿的潜在作用靶点及作用机制,并通过动物体内试验加以验证,为深入研究麻黄甘草汤的药理作用提供参考依据。【方法】通过中药系统药理学分析平台(TCMSP)数据库获取麻黄、甘草的活性成分及其作用靶点,利用GeneCards数据库收集肺水肿疾病的作用靶点,将麻黄甘草汤的成分作用靶点和肺水肿疾病靶点取交集,基于STRING数据库构建蛋白相互作用网络(PPI),使用Cytoscape 3.6软件构建成分-靶点网络图。利用DAVID数据库进行GO功能和KEGG通路富集分析。对获得的关键成分和核心靶点通过AutoDock Vina进行分子对接,用以佐证网络药理学预测结果。选用2%氯化铵构建小鼠肺水肿模型,分为空白对照组、氯化铵模型组及麻黄甘草汤治疗组;空白对照组每日上午腹腔注射200μL生理盐水,氯化铵模型组和麻黄甘草汤治疗组腹腔注射200μL 2%的氯化铵溶液;氯化铵模型组和空白对照组每晚灌胃200μL生理盐水,麻黄甘草汤治疗组灌胃200μL 1 g/mL麻黄甘草汤,连续处理5 d后采用实时荧光定量PCR检测白细胞介素-6(IL6)、诱导型一氧化氮合酶(NOS2)、丝裂原...     

Acute noncardiogenic pulmonary edema in an anesthetized Nubian goat kid

ObservationsA 1-month-old Nubian goat presented for sialocyst resection. Physical examination and bloodwork were unremarkable. While pre-oxygenating, the goat was sedated with midazolam and morphine (0.1 mg kg^?1 each) intravenously (IV). General anesthesia was induced 5 minutes later with 1.7 mg kg^?1 propofol. Sevoflurane was administered in oxygen without assisted ventilation via a cuffed orotracheal tube. Throughout the first 85 minutes of anesthesia, the goat was well-oxygenated (SpO₂, ≥97%), ventilating adequately (Pe′CO₂, 36–48 mmHg), and had normal mean arterial blood pressure (MAP, 60–85 mmHg). Blood-gas values at 45 minutes were consistent with adequate ventilation on oxygen. At 75 minutes, the goat moved in response to surgical stimulation, requiring additional propofol (0.4 mg kg^?1). After 10 minutes, MAP dropped precipitously to 40 mmHg and frequent multiform premature ventricular contractions (PVCs) were observed. Crystalloids, hetastarch, and dopamine (5 μg kg^?1 minute^?1) were administered to correct the hypotension. Arterial blood-gas analysis revealed that the goat had become hypoxemic (PaO₂, 50 mmHg). Intermittent positive pressure ventilation (IPPV) was initiated. Subsequent blood-gas analysis did not show significant improvement in PaO₂ (53 and 56 mmHg, respectively). Occasional PVCs were observed thereafter. Surgery ended, and sevoflurane and IPPV were discontinued. The goat was extubated within 7 minutes and received 100% oxygen by mask. Diffuse crackles were ausculted over both hemithoraces. Suspecting pulmonary edema, furosemide (1 mg kg^?1) was administered IV. Radiographs taken immediately post-operatively revealed a severe, caudodorsal airspace (alveolar) pattern, confirming the diagnosis. Respiration improved considerably within an hour with nasal oxygen and two additional doses of furosemide.ConclusionsThe goat developed acute, drug-induced, noncardiogenic pulmonary edema in response to the second dose of propofol.     

Acute respiratory distress syndrome in dogs and cats: a review of clinical findings and pathophysiology

Objective: To review the clinical and pathophysiologic aspects of acute respiratory distress syndrome (ARDS) in dogs and cats. Data sources: Data from human and veterinary literature were reviewed through Medline and CAB as well as manual search of references listed in articles pertaining to acute lung injury (ALI)/ARDS. Human data synthesis: Since the term ARDS was first coined in 1967, there has been a abundance of literature pertaining to this devastating syndrome in human medicine. More complete understanding of the complex interactions between inflammatory cells, soluble mediators (e.g., tumor necrosis factor, interleukin (IL)‐6, IL‐8, platelet activating factor) and the clinical patient has provided for timely recognition and mechanistically based protective strategies decreasing morbidity and mortality in human patients with ARDS. Veterinary data synthesis: Although little is known, ARDS is becoming a more commonly recognized sequela in small animals. Initial case reports and retrospective studies have provided basic clinical characterization of ARDS in dogs and cats. Additionally, information from experimental models has expanded our understanding of the inflammatory mechanisms involved. It appears that the inflammatory processes and pathologic changes associated with ARDS are similar in dogs, cats, and humans. Conclusions: Unfortunately, current mortality rates for ARDS in small animals are close to 100%. As our capability to treat patients with advanced life‐threatening disease increases, it is vital that we develop a familiarity with the pathogenesis of ARDS. Understanding the complex inflammatory interactions is essential for determining effective preventative and management strategies as well as designing novel therapies for veterinary patients.     

Toward quantification of loop diuretic responsiveness for congestive heart failure

Diuretics, such as furosemide, are routinely administered to dogs with congestive heart failure (CHF). Traditionally, dose and determination of efficacy primarily are based on clinical signs rather than quantitative measures of drug action. Treatment of human CHF patients increasingly is guided by quantification of urine sodium concentration (uNa) and urine volume after diuretic administration. Use of these and other measures of diuretic responsiveness is associated with decreased duration of hospitalization, complication rates, future rehospitalization, and mortality. At their core, loop diuretics act through natriuresis, and attention to body sodium (Na) stores and handling offers insight into the pathophysiology of CHF and pharmacology of diuretics beyond what is achievable from clinical signs alone. Human patients with low diuretic responsiveness or diuretic resistance are at risk for difficult or incomplete decongestion that requires diuretic intensification or other remedial strategies. Identification of the specific etiology of resistance in a patient can help tailor personalized interventions. In this review, we advance the concept of loop diuretic responsiveness by highlighting Na and natriuresis. Specifically, we review body water homeostasis and congestion in light of the increasingly recognized role of interstitial Na, propose definitions for diuretic responsiveness and resistance in veterinary subjects, review relevant findings of recent studies, explain how the particular cause of resistance can guide treatment, and identify current knowledge gaps. We believe that a quantitative approach to loop diuretic usage primarily involving natriuresis will advance our understanding and care of dogs with CHF.     

Pulmonary Edema Due to Oral Gavage in a Toxicological Study Related to Aquaporin-1, -4 and -5 Expression

A one-time oral gavage can be enough to cause of alveologenic edema with higher expression of AQP-1 and -4 than that with repeated-dose oral gavage, which caused both profound perivascular edema and hydrostatic pressure edema, while AQP-5 was similarly expressed. The alteration of AQPs expression was probably related to alveolar fluid clearance across the alveolar and bronchiolar epithelium in different stages of lung injury. The results clarified the type of lung edema in acute and sub-chronic toxicity studies without treatment related effect of tested material. The pathogenesis of pulmonary edema due to oral gavage toxicological study is associated with the cellular immune response to the reflux materials. Mast cell and leukocyte accumulation may contribute to increase vascular permeability leading to permeability edema. The increase in alveolar septum epithelium, perivascular and peribronchial cuffing, accumulation alveolar lipid containing macrophage and medial hyperplasia of the pulmonary artery might have been caused to increase airway resistance, which resulted in hydrostatic pressure edema.     

Traumatic brain injury: a review of pathophysiology and management

Objective – To review current information regarding the pathophysiology associated with traumatic brain injury (TBI), and to outline appropriate patient assessment, diagnostic, and therapeutic options. Etiology – TBI in veterinary patients can occur subsequent to trauma induced by motor vehicle accidents, falls, and crush injuries. Primary brain injury occurs at the time of initial impact as a result of direct mechanical damage. Secondary brain injury occurs in the minutes to days following the trauma as a result of systemic extracranial events and intracranial changes. Diagnosis – The initial diagnosis is often made based on history and physical examination. Assessment should focus on the cardiovascular and respiratory systems followed by a complete neurologic examination. Advanced imaging may be indicated in a patient that fails to respond to appropriate medical therapy. Therapy – Primary brain injury is beyond the control of the veterinarian. Therefore, treatment should focus on minimizing the incidence or impact of secondary brain injury. Because of a lack of prospective or retrospective clinical data, treatment recommendations for veterinary TBI patients are primarily based on human and experimental studies and personal experience. Therapeutic guidelines have been developed that center on maintaining adequate cerebral perfusion. Prognosis – Severe head trauma is associated with high mortality in humans and animals. However, dogs and cats have a remarkable ability to compensate for loss of cerebral tissue. It is therefore important not to reach hasty prognostic conclusions based on initial appearance. Many pets go on to have a functional outcome and recover from injury.     

Successful balloon angioplasty of pulmonary artery stenosis in two cats and associated complications

Two cats (2.5 months and 8 months old) were each evaluated due to a loud systolic murmur, and each was diagnosed with severe pulmonary artery stenosis at the bifurcation of the main pulmonary artery. Echocardiograms confirmed significant right atrial dilation and right ventricular dilation and/or hypertrophy that was progressive in one cat. Atenolol was initiated and the cats were referred for interventional therapy. Balloon angioplasty was performed via the jugular vein. In case 1, the pressure gradient across the stenosis was reduced from 169.7 mmHg to 23.6 mmHg and 52.4 mmHg across the left and right branch pulmonary arteries, respectively. In case 2, the stenotic echocardiographic gradient was reduced from 64 mmHg to 38.0 mmHg and 35.3 mmHg across the left branch and right-branched pulmonary arteries respectively. Both patients developed moderate to severe dynamic right ventricular outflow tract obstruction post angioplasty. Case 2 developed hypotension, desaturation, and ventricular arrhythmias intra-operatively. Case 1 was discharged but appeared to develop acute lung perfusion injury approximately 36 h after procedure that was manifested by radiographic pulmonary congestion and pulmonary infiltrate of the left lung fields. The congestion was successfully managed medically. Serial echocardiograms over the following 4 years in case 1 showed near complete resolution of the stenosis and associated right heart enlargement.     

Management of polyethylene glycol solution aspiration using bronchoscopic lavage in a dog

Polyethylene glycol lavage solutions are used for colonic preparation in dogs and are considered relatively safe. Aspiration is an uncommon but potentially devastating complication of polyethylene glycol administration. Full recovery is possible and often rapid in people treated with bronchoalveolar lavage. A healthy 2-year-old male Beagle used in an endoscopy teaching laboratory aspirated a small amount of polyethylene glycol lavage solution. Although initially appearing unaffected, the dog quickly became hypoxemic. Bronchoscopy was used to lavage the lungs and aspirate tracheal/pulmonary fluid 5 times over the course of 45 minutes. The dog completely recovered. This report presents the successful treatment of polyethylene glycol aspiration in a dog. Although the seriousness of aspiration might not be immediately evident, bronchoscopy and lavage should be pursued because of the rapidly progressive nature of polyethylene glycol-induced pulmonary edema.     

猪水肿病菌株毒素的抽提、鉴定和产毒量比较

对分离自江苏、上海等地的１５株仔猪水肿病菌株进行了毒素抽提，细胞毒性和动物试验鉴定结果表明，其中１４株能产生水肿病毒素（ＳＬＴ－Ⅱｖ），说明水肿病的发生与毒素密切相关。本文比较了这些菌株的产毒量，筛选出４株高产毒素菌株。     

Testing and Identification of Carp Edema Virus Disease in Cultured Koi

An acute infectious diseases occurred in a koi farm in Fangshan district, Beijing, and it resulted in mortalities of more than 50%.The main symptoms of sick koi were gills necrosis, kidney erosion and edema,which were similar to the clinical signs of koi herpes virus disease (KHVD).But PCR tests showed negative results for KHV. For further diagnosis, bacterial cultures, transmission electron microscopy studies, virus isolation and PCR tests were used. Electron microscopic observation revealed pox virus particles having a size of about 200 nm×400 nm in the kidney. 548 and 180 bp fragments were amplified from organs of sick koi by PCR method using specific primers of carp edema virus (CEV). The fragments were sequenced and analysed. The results showed that they were shared 100% nucleotide identity with CEV-H504. All the results indicated that this disease was carp edema virus disease, caused by a kind of pox virus, CEV. This was the first report on the CEV of cultured koi in China.     

养殖锦鲤鲤鱼浮肿病的检测与鉴定

北京房山某锦鲤养殖场锦鲤发生大量死亡,患病锦鲤呈烂鳃、肾脏糜烂、身体浮肿;症状类似锦鲤疱疹病毒（koi herpes virus,KHV）感染,但经PCR检测排除了KHV感染。为进一步确定病原,对发病鱼进行了临床症状观察、病毒分离、细菌分离培养、病鱼组织超薄切片电镜观察和PCR扩增等检测。通过病鱼组织超薄切片电镜观察,在肾脏内可见200 nm×400 nm的痘病毒样颗粒。抽提病毒核酸后,用已知的鲤鱼浮肿病毒（carp edema virus,CEV）的保守序列设计2对引物进行PCR扩增,扩增出548和180 bp片段,测序结果和GenBank公布的CEV H504株序列完全一致。根据发病鱼临床症状和实验室检测结果,最终确定该病为CEV引起的鲤鱼浮肿病。这是在中国首次发现的鲤鱼浮肿病。