新生仔犬溶血症的初步探讨

2006年8月31日,本基地一头母犬（2003年9月6目生）,顺利产下一窝小犬,共13头（10公3母）,其中2头小犬产下已经死亡,其他小犬状况良好,母乳颜色等较好,小犬正常喝母乳。但24小时后1头小犬突然死亡,几小时后又出现1头小犬死亡。饲养员发现2头小犬生前吃奶正常,但体重下降,精神状态不好,运动无力,死前出现抽搐,四肢挣扎后突然死亡。经过检查发现大多小犬可视粘膜黄染、皮肤口角发黄,     

新生仔犬假死的急救

仔犬产出后心脏跳动而呼吸障碍或无呼吸,或心跳、呼吸虽有,但昏睡不醒,统称新生仔犬假死或窒息,如急救不当常发生仔犬死亡。     

怎样避免新购幼犬应激反应综合征

新购幼犬易主后,由于突然间的改变地点、饮食、环境等因素,一周内易发生以消化系统和呼吸系统为主要症状的疾病,我们称为应激反应综合征。轻者易引起幼犬的身体发育不良或者其他疾病的并发症,重者可以导致幼犬的死亡。如何避免这种疾病?笔者认为首先应做好养犬前的准备工作。准备好犬的居住场所、饲喂用具和常用药品等。在购买时,一定要细心观察,切勿操之过急。为防止购入病犬,应注意幼犬的双眼眼睑无分泌物,眼球清洁,双眼有神,无上下眼睑内翻外翻等;双耳耳阔耳道内干净,无异物、异味;鼻镜湿润、冰凉,不干燥、不发热,嗅、视、听觉良好;皮肤…     

Acute respiratory distress syndrome.

Several combination therapies have been described throughout this article: in all likelihood, it is combination therapy that will allow improved survival of ARDS patients. As medicine moves into the future, clinical trials evaluating the efficacy of therapies for ARDS will be performed. In human critical care medicine, a large forward step was taken when ALI and ARDS were clearly defined. Unfortunately. as good as the definition is, ALI and ARDS occur secondary to many different underlying pathologic processes,perhaps obscuring the benefits of certain therapies for ARDS based on the underlying condition, for example, trauma versus sepsis. Selection of patients entering any ARDS trial is crucial: not only must those patients meet the strict definition of ARDS but the underlying disease process should be clearly identified. Identification of patients suffering from different disease processes before the onset of ARDS will allow for stratification of outcomes according to the intervention and the underlying pathology--comparing apples to apples and not to oranges. We are in a unique position in veterinary medicine. Although frequently financially limited by our clients, we have the opportunity to achieve several goals. First, we need to clearly define what constitutes ALI and ARDS in veterinary medicine. Do we want to rely on the human definitions? Probably not; however, as a group, we need to determine what we will accept as definitions. For example, we may not be able perform right heart catheterizations on all our patients to meet the wedge pressure requirement of human beings of less than 18 mm Hg. Do we agree that a PAOP of less than 18 mmHg is appropriate for animals, and is it appropriate for all animals? Will we accept another measure, for example, pulmonary artery diameter increases with echocardiographic evidence of acceptable left heart function? What is acceptable left heart function? As veterinarians, what do we consider to be hypoxemia? Is it the same in all species that we work with? What do we define as acute onset? Most human ARDS cases occur while patients are in hospital being treated for other problems, whereas many of our patients present already in respiratory distress. If we are unable to ventilate patients for economic or practical reasons, what do we use as the equivalent of the Pao2/Flo, ratio'? Reliance on the pathologist is not reasonable, because many disease processes can look similar to ARDS under the microscope. If anything, ALI and ARDS are clinical diagnoses. It is time for veterinarians to reach a consensus on the definition for ALI and ARDS in our patients.Only when we have a consensus of definition can rational prospective clinical trials of therapies be designed.     

Neonatal respiratory distress syndrome in the calf

Thirty-five calves were delivered by caesarean section near to term. During the operation amniotic fluid was collected for determination of the lecithin/sphingomyelin (L/S) ratio. Clinical examination of the calves and analysis of blood gas concentration (venous blood) were carried out within the first hour of life. Fifteen out of 35 calves under examination did not show clinical or blood gas disorders in the course of the first hour of life. In these calves, the L/S ratio, which represents a measure for the maturity of the surfactant system, averaged 2.6. The other 20 calves, however, developed a respiratory distress syndrome together with a progressive respiratory and metabolic acidosis within the first hour of life. The L/S ratio in the animals affected with respiratory distress syndrome reached an average value of 1.5 which was significantly below that of the calves not suffering from respiratory distress. Eleven of the 20 calves which developed respiratory distress syndrome died within the first 60 hours of life. The most striking findings in the post mortem examinations of these animals were intracranial haemorrhages and pulmonary lesions (hyaline membranes, interstitial and alveolar oedema). On the basis of the significantly lower L/S ratio and the post mortem findings, it is to be assumed that the respiratory distress syndrome in calves, equally with that in infants, is attributable to a surfactant deficiency.     

Developments in management of the newborn foal in respiratory distress 2: Treatment

New developments in therapy for foals in respiratory distress are discussed. Therapy is based on preservation of the foal's life by maintenance of a patent airway, resuscitation with fluids and warmth, provision of humidified oxygen to raise the fractional concentration of inspired oxygen sufficient to avoid hypoxia and provision of ventilatory support when hypercapnia becomes critical. Ventilatory support described includes assisted and controlled ventilation, positive end expiratory pressure, continuous positive airway pressure and intermittent mandatory ventilation. The aims of these techniques are discussed together with their associated indications, disadvantages and complications. Secondary therapy includes coupage, airway hygiene, drug therapy and stress management. Knowledge of equine neonatology is limited in comparison with human neonatology. More information in basic physiology and pharmacology relating to equine neonatology is needed and the efficacy of various modes of therapy must be evaluated.     

Developments in management of the newborn foal in respiratory distress 1: Evaluation

Developments in evaluation of newborn foals with respiratory distress are discussed. Major causes of respiratory distress are outlined and discussed in terms of the similar respiratory signs exhibited by foals with this clinical syndrome. History, physical examination, clinical pathology, chest radiography and blood gas analyses are discussed as important elements of the evaluation of the condition of these foals. Foals with respiratory disease are grouped into three major categories on the basis of clinical signs and arterial blood gas profiles. The evaluation of foals with respiratory distress is designed not only to reach an accurate diagnosis of the aetiology but also to define the foal's need for respiratory support.     

Acute respiratory distress syndrome in an alpaca cria

A 7-hour-old alpaca was presented for lethargy and depression. The cria responded favorably to initial treatment but developed acute-onset dyspnea 48 hours later. Acute respiratory distress syndrome was diagnosed by thoracic imaging and blood gas analysis. The cria was successfully treated with corticosteroids and discharged from the hospital.     

弱胎仔犬浅议

弱胎是在犬的繁殖过程中经常遇到的问题。部分初生仔犬在体重、体质、哺乳能力和抗逆性等方面弱于正常仔犬,生活能力低下,死亡几率较高,我们把这部分仔犬称为弱胎仔犬。据不完全统计,弱胎仔犬占仔犬总数10%～20%左右。当同窝仔犬总数在5个以下时,弱胎现象表现得并不明显,同窝仔     

Brodifacoum toxicosis in two neonatal puppies

Eight out of a litter of 13 puppies were either born dead or died within 48 hours of birth. Three puppies that died shortly after birth were necropsied. Two puppies had hemorrhage in the thoracic and peritoneal cavities, intestinal serosa, and meninges. The third puppy was smaller than the other two puppies but did not have detectable hemorrhage. Brodifacoum, a second-generation coumarin anticoagulant, was detected in livers from the two puppies with hemorrhage. The dam did not have clinical signs of coagulopathy before or subsequent to whelping. The owners were confident that the dog had not been exposed to rodenticide for at least 4 weeks before whelping. A presumptive diagnosis of in utero brodifacoum toxicity was made. To the authors' knowledge this is the first time a second-generation coumarin anticoagulant has been detected in the liver of a newborn animal. This case is also unique because the dam was unaffected, suggesting that fetuses are more susceptible to brodifacoum toxicity than adult animals.     

Congenital hypothyroidism in Scottish Deerhound puppies

Two Scottish Deerhound puppies had clinical and pathological features consistent with the diagnosis of congenital non-goitrous hypothyroidism. They were from separate litters, but were the progeny of the same sire and dam. The puppies were smaller, had shorter limbs and shorter, broader heads than their littermates. They also had histories of weakness, difficulty in walking and somnolence. A characteristic radiographic feature was the absence of epiphyseal growth centres. Both had depressed serum thyroxine (T4) levels and one did not respond to exogenous thyroid stimulating hormone. On necropsy, the thyroid glands were small, the follicles varied in size and contained little or no colloid. The adenohypophysis contained many cells with markedly vacuolated cytoplasm. It is suggested that the clinicopathological pattern is the result of a primary thyroid abnormality. Possible mechanisms include either primary thyroid hypoplasia or an unresponsiveness to thyroid stimulating hormone.