Testicular ischaemic necrosis as a cause of equine cryptorchidism

2016 ◽  
Vol 29 (6) ◽  
pp. 314-317 ◽  
Author(s):  
A. K. Gardner ◽  
E. M. Santschi ◽  
F. Aeffner ◽  
J. H. Pigott ◽  
D. S. Russell
Keyword(s):  
Ischaemic Necrosis

scholarly journals One-Stop Outpatient Management of Accessory Auricle in Children with Titanium Clip

2014 ◽  
Vol 2014 ◽  
pp. 1-4 ◽  
Author(s):  
Phui Yee Wong ◽  
Tereze Laing ◽  
Catherine Milroy
Keyword(s):  
Complication Rate ◽  
Surgical Excision ◽  
Outpatient Setting ◽  
Patient Records ◽  
Outpatient Management ◽  
Suture Ligation ◽  
One Stop ◽  
Ischaemic Necrosis ◽  
Telephone Questionnaire

Introduction. Literature on ideal management of accessory auricles is limited. Traditionally, accessory auricles are managed by paediatricians with suture ligation at the base of the accessory auricle to induce ischaemic necrosis (Mehmi et al, 2007). This method can be associated with complications and poor cosmesis thus leading to the vogue of surgical excision ( Frieden et al, 1995; Sebben, 1989). We present our experience in managing these lesions in children with the application of a titanium clip in a one-stop outpatient setting. Methods. Data was collected retrospectively through review of patient records and telephone questionnaire identifying outcomes from the parents’ perspective. Results. Of 42 patients, 24 (57.1%) responded. Eleven (26.2%) underwent surgical excision, 6 (14.3%) had no intervention, and 1 (2.4%) was not contactable. All parents were happy with the outcome and would recommend this management to other parents. Twenty-three (96%) had no complications apart from a tiny residual nubbin, which was considered cosmetically acceptable. One child had a residual nubbin that grew in size requiring surgical excision at later stage. Conclusion. Management of accessory auricles by the application of a titanium clip in one-stop outpatient setting is safe, simple, quick, and well tolerated with no need for admission, anaesthesia, or followup due to the low complication rate.

HISTOLOGICAL ALTERATIONS IN THE RAT PITUITARY TRANSPLANTED TO THE EYE

1961 ◽  
Vol 23 (2) ◽  
pp. 109-117 ◽  
Author(s):  
K. KOVÁCS
Keyword(s):  
Pituitary Gland ◽  
Anterior Chamber ◽  
Functional Activity ◽  
Anterior Pituitary ◽  
Peripheral Zone ◽  
Necrotic Area ◽  
Histological Alterations ◽  
Rat Pituitary ◽  
Intraocular Grafts ◽  
Ischaemic Necrosis

SUMMARY Homotransplantation of the anterior pituitary gland of rats was made into the anterior chamber of the eye. The centre of the grafts developed ischaemic necrosis, but the peripheral zone remained alive to a depth of about 100 μ. During the next 6 weeks there was no evidence of significant regeneration or atrophy of this live peripheral zone, and mitoses were not observed there. The gradual resorption and scarring of the central necrotic area led to a diminution of the overall size of the graft. In the surviving tissue nearly all the chromophil cells became completely degranulated during the first week or two. After 6 weeks only very rare shrunken basophil cells remained, although a few acidophil cells could still be identified. From previous work it is known that such intraocular grafts have very little functional activity. This may possibly be because of the absence of any direct connexion between the graft and the hypothalamus, but the reduction of the total amount of parenchyma may also be an important factor.

Recurrent hypoglycaemia and dilated cardiomyopathy: delayed presentation of Sheehan’s syndrome

2021 ◽  
Vol 14 (6) ◽  
pp. e242747
Author(s):  
Archita Makharia ◽  
Manoj Lakhotia ◽  
Vineet Tiwari ◽  
Kishan Gopal
Keyword(s):  
Dilated Cardiomyopathy ◽  
Clinical Manifestations ◽  
Diabetic Woman ◽  
Delayed Presentation ◽  
Sheehan’S Syndrome ◽  
Life Threatening ◽  
History Of ◽  
Sheehan's Syndrome ◽  
Ischaemic Necrosis ◽  
Recurrent Hypoglycaemia

Sheehan’s syndrome (SS) is ischaemic necrosis of the pituitary gland due to massive postpartum haemorrhage. The clinical manifestations may vary from subtle to life-threatening and may present immediately after delivery or many years later. We present a case history of a 58-year-old non-diabetic woman who had undetected SS and presented with two unusual manifestations, including recurrent hypoglycaemia and dilated cardiomyopathy 34 years after delivery. The dilated cardiomyopathy reversed partially after treatment.

Avascular necrosis

2013 ◽  
pp. 1266-1273
Author(s):  
Stefan Rehart ◽  
Martina Henniger
Keyword(s):  
Avascular Necrosis ◽  
Femoral Condyle ◽  
Clinical Signs ◽  
Disease Process ◽  
Core Decompression ◽  
Underlying Disease ◽  
Classification Systems ◽  
Circulatory Disorder ◽  
Ischaemic Necrosis ◽  
Important Disease

Avascular necrosis (AVN) represents an important disease process of the cartilage-bone complex, which can occur at any age. According to aetiology one may discriminate between rare idiopathic avascular necroses and more common forms that occur as an effect of the underlying disease or rather the therapy, the secondary avascular necroses. Pathophysiologically it is assumed that a circulatory disorder leads to an ischaemic necrosis of bone, bone marrow, and adjunct cartilage. Sites of the human skeleton with predilection to AVN are the femoral head, humeral head, femoral condyle, proximal tibia, and ossicles of the foot and hand. Clinical signs are unspecific, but in the region of the load-bearing lower extremities pain occurs usually early. Plain radiographs, MRI, and sometimes also skeletal scintigraphy are used for diagnosis and staging. Usually 4-5 stages are distinguished; there are extra classification systems for individual entities. Spontaneous healing in terms of a return to normal without further damage can be found in small, circumscribed areas, but the bigger and the nearer the joint the more unlikely this is. Depending on region, stage of disease, age of the patient, concomitant diseases and cause, several conservative and surgical therapies may be applied. Conservative treatments include exoneration and relief of the extremity, physiotherapy, and if necessary medical treatment. The need for surgical intervention becomes more likely as AVN increases in size and gets closer to the joint. Surgical therapies include core decompression, revascularizing techniques, vascular bone transplant, corrective/transposition osteotomy, arthrodesis/joint reinforcement, or joint replacement.

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