scholarly journals Atresia Ani (Imperforated Anus) in Calves: Clinical, Surgical and Pathological Aspects

2021 ◽  
Vol 49 ◽  
Author(s):  
Maria Eduarda Dos Santos Lopes Fernandes ◽  
Saulo Andrade Caldas ◽  
Letícia Ramos Rocha ◽  
Marina Galindo Chenard ◽  
Kelly Regina Freitas Freire ◽  
...  

Background: Anal atresia is a congenital malformation, which often affects calves, and is related to the imperforation of the membrane that separates the endoderm of the posterior intestine from the ectodermal anal membrane. It is commonly associated with other congenital malformations and skeletal anomalies. The clinical signs generally appear in the first days of the animal's life, due to a retention of feces. The diagnosis is clinical and is based on observation, anamnesis and a physical examination of the animal. The only viable treatment is surgical. This paper aims to report 6 cases of anal atresia in bovine calves, 4 males and 2 females that were successfully treated surgically. Cases: This work reports 6 cases of anal atresia in 4 male calves and 2 female calves. Three presented total atresia (type II), one partial (type I) and in both female calves, anal atresia and rectovaginal fistula (type IV) were observed. The animals were all of undefined race. Five of the cases were from northern Tocantins, 4 males and 1 female (anal atresia with rectovaginal fistula), and 1 female (anal atresia with rectovaginal fistula) was from Valença, RJ. All animals were born active, by eutocic/natural birth, and assumed a quadrupedal position followed by the first feeding as normal. They were aged between 2 days and 6 months, and had a clinical history of abdominal distention and difficulty or inability defecating, and the females both also had a rectovaginal fistula, all cases compatible with anal atresia. Based on the patient's history and clinical examination, surgical treatment for anal reconstruction was decided upon. Postoperative treatment consisted of enrofloxacin [2.5 mg/kg - intramuscularly (IM), once daily (SID), for 5 days] and fluxinin meglumine [1.1 mg/kg - IM, SID, for 3 days] ; as well as a healing ointment which was applied to the area of the surgical wound, every 12 h, for 7 days. There were no trans-surgical complications. The animals showed progressive recovery after anal reconstruction and the stitches were removed in all cases on the 10th postoperative day, with no postoperative complications and no recurrence of any clinical signs from that moment on.Discussion: The study of congenital and hereditary changes enables the identification of their origins, can help prevent new cases and, some of them, are open to economically viable treatment and/or correction that can improve the well-being of the animal and prevent economic losses due to death or animal sacrifice, as reported in the present study. Anal atresia is the most common congenital defect of the lower gastrointestinal tract in calves, being an isolated abnormality, or associated with other malformations, especially of the distal spinal column such as the absence of a tail (perosumus acaudato), as one of the animals in this study. The clinical signs and physical examination are sufficient to establish the diagnosis, as demonstrated in this report, which is usually made in newborn animals, due to the lack or difficulty in defecation associated with no anal orifice and/or swelling in the perineal region. The treatment of choice for anal atresia is surgical, in order to construct an anal neo-orifice and thus avoid endotoxemic shock as well as providing relief and well-being for the animals. As observed in this study, when anal atresia is diagnosed early, and surgical treatment is properly instituted, the prognosis is favorable. The surgery is considered of low complexity, quick and it can be carried out in the field. Thus, from a commercial point of view, considering the costs of the procedures and the value of the calf at the end of weaning, such treatments are beneficial to the owners. In addition, the surgical treatment is essential for animal health and welfare in cases of anal atresia.Keywords: cattle, congenital defects, hereditary pathology, perosomus acaudato, surgery.

2020 ◽  
Vol 48 ◽  
Author(s):  
Maria Eduarda Dos Santos Lopes Fernandes ◽  
Luiza De Albuquerque Carvalho ◽  
Marina Galindo Chenard ◽  
Cícero Araújo Pitombo ◽  
Orlei Justen Dos Santos ◽  
...  

Background: Flexural deformities are anatomical deviations, in varying degrees, of one or more joints, and may have a congenital or acquired origin. Congenital contracture of the deep digital flexor tendon (DDFT) affects newborn calves and results in hyperflexion of the metacarpal-phalangeal joint, which in severe cases means that the animal must support its own weight on its fetlock joints. The aim of this study is to report the rapid and successful result of applying bilateral total tenotomy technique on a newborn bovine that had been diagnosed with severe bilateral DDFT contracture in the thoracic limbs.Case: A 3-week-old male bovine with a history of difficulty in maintaining a quadrupedal position was attended at the Veterinary Hospital of the Federal University of Tocantins. The animal had severe bilateral locomotor alterations in the thoracic members to the point that he walked on his fetlock joints. The physical examination revealed clinical parameters within the normal range. However, the locomotor system examination showed severe flexor deformity in the bilateral metacarpal-phalangeal joints, and the limbs were being supported on the dorsal face of the fetlock joints, which presented ulcerations, and was suggestive of a shortening of the DDFT. Based on the patient's history and clinical examination, as well as the severity of the tendon contractures, surgical treatment using the DDFT bilateral total tenotomy technique was decided upon. Postoperative treatment consisted of 2.5 mg/kg of enrofloxacin intramuscularly (IM), SID, for 5 days and 0.5 mg/kg meloxicam via IM, SID, for 3 days; as well as a dressing (cotton, medical bandage and a PVC mold) on the thoracic limbs to provide support and allow the animal to walk, until its complete recovery. One day after the surgery, the animal was able to walk with difficulty and some trembling; however, on the third day after the surgical procedure, it could stand up by itself, walk and graze normally. The surgical stitches were removed seven days after the operation, as the surgical wounds had healed adequately. The animal was followed-up for a one-month period after the total tenotomy, with no recurrence of any of the clinical signs, and the thoracic limbs had regained normal biomechanics.Discussion: Congenital flexural deformities are common in newborn calves of different breeds and their incidence is mainly in the thoracic limbs, especially in the carpal, distal interphalangeal and metacarpal-phalangeal joints as was reported in the animal in this study. The history and anamnesis of the animal, along with a thorough physical examination, in order to rule out any other congenital alterations, was extremely important in the diagnosis, and the classification of the severity of the deformity along with the choice of appropriate treatment in the present study. Although total tenotomy is rarely reported in the literature, and there are controversial results with calves, the surgical treatment was chosen in the present case due to the severity of the case. The DDFT bilateral total tenotomy surgical technique gave satisfactory results for the correction of severe bilateral flexor deformity in the thoracic limbs of the newborn crossbred calf. Complete recovery of the limb biomechanics was rapid, and there was no post-surgical complications, thus ensuring the animal could have a good and healthy life. Total DDFT tenotomy is considered a viable surgical procedure for calves with severe congenital flexor deformities; however, post-operative care is also important to ensure good final results.


2013 ◽  
Vol 33 (5) ◽  
pp. 495-502 ◽  
Author(s):  
Joerg Latus ◽  
Christoph Ulmer ◽  
Peter Fritz ◽  
Bianka Rettenmaier ◽  
Dagmar Biegger ◽  
...  

BackgroundEncapsulating peritoneal sclerosis (EPS) is a rare but devastating complication of peritoneal dialysis (PD), with clinical signs of abdominal pain, bowel obstruction, and weight loss in late stages.MethodsWe retrospectively analyzed all patients who were diagnosed with EPS between March 1998 and October 2011 in our department of nephrology. We focused on the 24 EPS patients who underwent surgery because of symptomatic late-stage EPS. We identified 3 different macroscopic phenotypes of EPS that we categorized as types I – III. We correlated histologic findings with those macroscopic phenotypes of EPS. The postoperative and long-term outcomes were evaluated by macroscopic phenotype.ResultsDuration of PD was longer in type III than in types I and II EPS ( p = 0.05). We observed no other statistically significant differences between the groups in baseline characteristics, except for operation time, which was longer in the type I than in the type III group ( p = 0.02). Furthermore, we observed no statistically significant difference between the groups with respect to the onset of complaints before surgery (7.8 ± 5.9 months vs 7.0 ± 7.0 months vs 6.5 ± 5.3 months). Concerning patient outcomes, there was no evidence that any of the macroscopic EPS types was associated with more major or minor complications after surgery. For all study patients, follow-up was at least 3 years, with 19 patients still being alive, and 16 having no or very mild complaints. The typical histologic findings of EPS were present in all macroscopic types; only fibrin deposits were more prominent in type II than in type III.ConclusionsWe describe 3 subtypes of EPS based on macroscopic findings. Postoperative treatment should probably not be influenced by the macroscopic EPS phenotype. Whether the different phenotypes represent different pathophysiologic processes remains unclear and has to be further evaluated.


2018 ◽  
Vol 63 (No. 4) ◽  
pp. 175-180
Author(s):  
A. Foglia ◽  
S. Del Magno ◽  
M. Pietra ◽  
V. Cola ◽  
M. Joechler ◽  
...  

A 7-year-old intact male Rottweiler dog was evaluated for recurrent dysphagia and regurgitation. Physical examination was unremarkable and routine blood works were within normal limits. Computed tomography revealed a defined lesion in the caudal mediastinum arising from the oesophagus. The lesion was excised using intercostal thoracotomy and the histological diagnosis was oesophageal duplication cyst. The dog recovered uneventfully and at a 3-year follow-up no clinical signs were reported. Although extremely rare, oesophageal duplication cysts should be considered in the differential diagnosis in cases of chronic regurgitation and dysphagia associated with evidence of an oesophageal lesion.


2018 ◽  
Vol 17 (2) ◽  
pp. 65-70
Author(s):  
I. O. Kozak ◽  
S. R. Mykytyuk ◽  
V. P. Mosiychuk ◽  
L. I. Kozak

The article presents the review of the literature and own clinical observations on the diagnosis and surgical treatment of Mirizzi syndrome – a rare complication of gallstones. The clinical features of the disease has no specific symptoms. The main clinical signs of MS are periodic jaundice (84%), pain in the right hypochondrium (75%) and cholangitis (56%), the phenomenon of acute cholecystitis and pancreatitis. The most informative method of preoperative diagnosis is magnetic resonance imaging, which, unfortunately, not readily available for public use. The diagnostic sensitivity of MRI with MS is 97,6%, intraoperative cholangiography – 94%, ERCP – 86%, PTC – 5%, fibrocholangioscopy – 77%, ultrasound – 46%. The most common type of MS (10,5-51%), less often type II (15-41%), even more rare types III (3-44%), IV (7,4%) and V (2,9% ). The leading role in the treatment of syndrome belongs to open surgery. Laparoscopic cholecystectomy can only be shown to individual MS and type I patients. Conversion with this occurs in 31-100%, complications – 60%, damage to common bile duct – 22%. Open cholecystectomy remains the standard. For Type II and III types of MS, they perform cholecystectomy while retaining part of the Hartmann pocket with the subsequent plastics of CBD at the Kehr drainage. At type IV of the MS it is shown a hepaticojejunostomy. Reorder phases of operation including cholangiography before cholecystectomy made it possible to diagnose and set the type of Mirizzi syndrome, to determine the optimal surgery approach and to prevent intra– and postoperative complications.


2019 ◽  
Vol 38 (1) ◽  
Author(s):  
Oksana Kamenskaya ◽  
Asya Klinkova ◽  
Irina Loginova ◽  
Alexander Chernyavskiy ◽  
Dmitry Sirota ◽  
...  

Author(s):  
А.Р. Зарипова ◽  
Л.Р. Нургалиева ◽  
А.В. Тюрин ◽  
И.Р. Минниахметов ◽  
Р.И. Хусаинова

Проведено исследование гена интерферон индуцированного трансмембранного белка 5 (IFITM5) у 99 пациентов с несовершенным остеогенезом (НО) из 86 неродственных семей. НО - клинически и генетически гетерогенное наследственное заболевание соединительной ткани, основное клиническое проявление которого - множественные переломы, начиная с неонатального периода жизни, зачастую приводящие к инвалидизации с детского возраста. К основным клиническим признакам НО относятся голубые склеры, потеря слуха, аномалия дентина, повышенная ломкость костей, нарушения роста и осанки с развитием характерных инвалидизирующих деформаций костей и сопутствующих проблем, включающих дыхательные, неврологические, сердечные, почечные нарушения. НО встречается как у мужчин, так и у женщин. До сих пор не определена степень генетической гетерогенности заболевания. На сегодняшний день известно 20 генов, вовлеченных в патогенез НО, и исследователи разных стран продолжают искать новые гены. В последнее десятилетие стало известно, что аутосомно-рецессивные, аутосомно-доминантные и Х-сцепленные мутации в широком спектре генов, кодирующих белки, которые участвуют в синтезе коллагена I типа, его процессинге, секреции и посттрансляционной модификации, а также в белках, которые регулируют дифференцировку и активность костеобразующих клеток, вызывают НО. Мутации в гене IFITM5, также называемом BRIL (bone-restricted IFITM-like protein), участвующем в формировании остеобластов, приводят к развитию НО типа V. До 5% пациентов имеют НО типа V, который характеризуется образованием гиперпластического каллуса после переломов, кальцификацией межкостной мембраны предплечья и сетчатым рисунком ламелирования, наблюдаемого при гистологическом исследовании кости. В 2012 г. гетерозиготная мутация (c.-14C> T) в 5’-нетранслируемой области (UTR) гена IFITM5 была идентифицирована как основная причина НО V типа. В представленной работе проведен анализ гена IFITM5 и идентифицирована мутация c.-14C>T, возникшая de novo, у одного пациента с НО, которому впоследствии был установлен V тип заболевания. Также выявлены три известных полиморфных варианта: rs57285449; c.80G>C (p.Gly27Ala) и rs2293745; c.187-45C>T и rs755971385 c.279G>A (p.Thr93=) и один ранее не описанный вариант: c.128G>A (p.Ser43Asn) AGC>AAC (S/D), которые не являются патогенными. В статье уделяется внимание особенностям клинических проявлений НО V типа и рекомендуется определение мутации c.-14C>T в гене IFITM5 при подозрении на данную форму заболевания. A study was made of interferon-induced transmembrane protein 5 gene (IFITM5) in 99 patients with osteogenesis imperfecta (OI) from 86 unrelated families and a search for pathogenic gene variants involved in the formation of the disease phenotype. OI is a clinically and genetically heterogeneous hereditary disease of the connective tissue, the main clinical manifestation of which is multiple fractures, starting from the natal period of life, often leading to disability from childhood. The main clinical signs of OI include blue sclera, hearing loss, anomaly of dentin, increased fragility of bones, impaired growth and posture, with the development of characteristic disabling bone deformities and associated problems, including respiratory, neurological, cardiac, and renal disorders. OI occurs in both men and women. The degree of genetic heterogeneity of the disease has not yet been determined. To date, 20 genes are known to be involved in the pathogenesis of OI, and researchers from different countries continue to search for new genes. In the last decade, it has become known that autosomal recessive, autosomal dominant and X-linked mutations in a wide range of genes encoding proteins that are involved in the synthesis of type I collagen, its processing, secretion and post-translational modification, as well as in proteins that regulate the differentiation and activity of bone-forming cells cause OI. Mutations in the IFITM5 gene, also called BRIL (bone-restricted IFITM-like protein), involved in the formation of osteoblasts, lead to the development of OI type V. Up to 5% of patients have OI type V, which is characterized by the formation of a hyperplastic callus after fractures, calcification of the interosseous membrane of the forearm, and a mesh lamellar pattern observed during histological examination of the bone. In 2012, a heterozygous mutation (c.-14C> T) in the 5’-untranslated region (UTR) of the IFITM5 gene was identified as the main cause of OI type V. In the present work, the IFITM5 gene was analyzed and the de novo c.-14C> T mutation was identified in one patient with OI who was subsequently diagnosed with type V of the disease. Three known polymorphic variants were also identified: rs57285449; c.80G> C (p.Gly27Ala) and rs2293745; c.187-45C> T and rs755971385 c.279G> A (p.Thr93 =) and one previously undescribed variant: c.128G> A (p.Ser43Asn) AGC> AAC (S / D), which were not pathogenic. The article focuses on the features of the clinical manifestations of OI type V, and it is recommended to determine the c.-14C> T mutation in the IFITM5 gene if this form of the disease is suspected.


2020 ◽  
pp. 97-99
Author(s):  
U. V. Kukhtenko ◽  
O. A. Kosivtsov ◽  
L. A. Ryaskov ◽  
E. I. Abramian

A clinical case of successful surgical treatment of a patient with a giant cervical retrosternal nontoxic goiter with severe cardiac pathology is presented. Thyroidectomy from cervical access without sternotomy was performed. At the follow-up examination 5 months after the operation, instrumental and clinical signs of disease relapse were not detected.


Animals ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 1670
Author(s):  
Gerald Reiner ◽  
Josef Kuehling ◽  
Frederik Loewenstein ◽  
Mirjam Lechner ◽  
Sabrina Becker

Tail biting is a prevalent and undesirable behaviour in pigs and a major source of significant reduction in well-being. However, focusing on biting considers only one part of the solution, because tail damage can be found with a high prevalence without any action by other pigs. The lesions are not limited to the tail but can also be found in the ears, heels, soles, claw coronary bands, teats, navel, vulva, and face. Environmental improvement alone often fails to overcome the problem. This review addresses a new inflammation and necrosis syndrome in swine (SINS). It shows the clinical signs and the frequencies of occurrence in different age groups. It compiles scientific evidence from clinical and histopathological studies in newborn piglets that argue for a primary endogenous aetiology of the disease. Bringing together the findings of a broad body of research, the possible mechanisms leading to the disease are identified and then discussed. This part will especially focus on microbe-associated molecular patterns in the circulation and their role in activating defence mechanisms and inflammation. Finally, the methods are identified to ameliorate the problem by optimizing husbandry and selecting a suitable breeding stock.


1986 ◽  
Vol 20 (2) ◽  
pp. 121-126 ◽  
Author(s):  
S. D. Sutherland ◽  
J. D. Almeida ◽  
P. S. Gardner ◽  
M. Skarpa ◽  
J. Stanton

During 1983 a severe episode of respiratory infection occurred in a marmoset colony at these laboratories. Of 91 marmosets, 69 showed clinical signs of disease, one died and nine were so ill that euthanasia was necessary. Eight were examined post mortem and all showed consolidation of the lungs. Laboratory studies were carried out in an attempt to establish the cause of the outbreak and an interstitial pneumonia was found in seven animals which were examined histologically. Direct electron microscopy of nasal swabs and lung samples revealed the presence of a high titre of a paramyxovirus, and subsequent immunofluorescence studies established that the particular paramyxovirus involved was parainfluenza virus type I. Subsequent studies showed that surviving affected animals had seroconverted to parainfluenza I virus while animals that had not been implicated in the outbreak had not.


PEDIATRICS ◽  
1959 ◽  
Vol 24 (2) ◽  
pp. 330-337
Author(s):  
Lytt I. Gardner ◽  
Ira M. Rosenthal ◽  
Richard J. Feinberg

Dr. Gardner: Historically pediatricians have been in the vanguard of the social and scientific forces improving the health and well-being of their patients—the children of this country. Indeed, we have the heavy responsibility of carrying on the proud tradition of our professional great-grandfather, Dr. Abraham Jacobi, who came to these shores in the aftermath of the German Revolution of 1848, and who eventually rose to the presidency of the American Medical Association. As the pioneer in American pediatrics, Jacobi never failed to let his position be known on controversial issues. His intuitive Jeffersonian grasp of the democratic process facilitated his rôle in the early development of pediatrics here. Jacobi's coat has, in a sense, fallen upon our shoulders, and American pediatrics must continually be on the alert to live up to what he would have expected of us. Therefore let me come directly to the problem at hand. As we know, the relative number of children with congenital defects in our hospitals is very much greater than 25 years ago. Recently in our hospital we tabulated the cases over a 5-month period, and found that 30% of the pediatric inpatients were there because of congenital defects. This apparent increase is almost certainly due in large part to the reduction in patients with infectious disease, but the figure of 30% still must remind us that the care of children with congenital defects is a field of major importance in modern pediatrics. How many of these defects are genetically determined is not known for sure, but certainly a considerable part of this group of patients represents inherited disease. As is obvious from the syndromes we will take up in this endocrine round table, nearly every one of these conditions is genetically determined, that is to say, the result of a mutation which has taken place in the human hereditary material.


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