Does surgical timing affect the rapidity of recovery in deep pain-entire non-ambulatory dogs with thoracolumbar intervertebral disk extrusion?

OBJECTIVE: To investigate whether the delay between onset of neurological signs and spinal cord decompression affects the time to recovery in non-ambulatory paraparetic/paraplegic dogs with deep pain perception affected by thoracolumbar intervertebral disc extrusion. MATERIALS AND METHODS: Data on non-ambulatory dogs with preserved deep pain perception in both hindlimbs and surgically treated for thoracolumbar intervertebral disc extrusion were prospectively collected from three referral hospitals. Cox proportional hazards regression was used to explore the relationship of time until restoration of independent ambulation with age, weight, preoperative use of anti-inflammatory drugs, delay between onset of inability to walk and arrival at the clinic, time between presentation and spinal surgery and surgery time. RESULTS: One hundred and fifty-one dogs were included. Median time from admission to surgery, including imaging, was 180 (interquartile range, 65.4 to 240) minutes. All dogs were operated within 72 hours. Follow-up was available for all 151 dogs and ranged from 1 to 21 months. All but three dogs, which were all grade IV at presentation, recovered the ability to ambulate. In both univariable and multivariable models, only duration of surgery and neurological (Frankel) grade at presentation were significantly associated with the rapidity of recovery of ambulation. CLINICAL SIGNIFICANCE: Delay between onset of clinical signs and presentation and time between presentation and spinal surgery was not associated with the rapidity of recovery of ambulation in dogs surgically treated for thoracolumbar intervertebral disc extrusion. These results should be evaluated in the context of a limited range of delay since only 14.5% dogs had a delay ≥6.5 hours. Duration of surgery and neurological grade at presentation were significantly associated with rapidity of recovery of ambulation.

ABCB1 c.-6-180T>G polymorphism and clinical risk factors in a multi-breed cohort of dogs with refractory idiopathic epilepsy.

Epilepsy is the most common chronic neurological disorder in dogs. Approximately 20-30% of dogs do not achieve satisfactory seizure control with two or more anti-epileptic drugs at appropriate dosages. This condition, defined as refractory epilepsy, is a multifactorial condition involving both acquired and genetic factors. The P glycoprotein might play and important role in the pathophysiological mechanism and it is encoded by the ABCB1 gene. An association between a single nucleotide variation of the ABCB1 gene (c.-6-180T>G) and phenobarbital resistance has previously been reported in a Border collie population with idiopathic epilepsy. To date, the presence and relevance of this polymorphism has not been assessed in other breeds. A multicentre retrospective, case-control study was conducted to investigate associations between ABCB1 c.-6-180T>G, clinical variables, and refractoriness in a multi-breed population of dogs with refractory idiopathic epilepsy. A secondary aim was to evaluate the possible involvement of the ABCB1 c.-6-180T>G single nucleotide variation this population. Fifty-two refractory and 50 responsive dogs with idiopathic epilepsy were enrolled. Of these, 45 refractory and 50 responsive (control) dogs were genotyped. The G allele was found in several breeds, but there was no evidence of association with refractoriness (P=0.69). The uncertain role of the c.-6-180T>G variation was further suggested by an association between the T/T genotype with both refractoriness and responsiveness in different breeds. Furthermore, high seizure density (cluster seizure) was the main clinical risk factor for refractory idiopathic epilepsy (P=0.003).

[Acute appendicitis. Experimental model in rabbits]. / Apendicite aguda. Modelo experimental em coelhos.

The evolving phases of acute appendicitis were studied experimentally. Sixty female rabbits (Oryctogalus cuniculus) of New Zealand lineage weighing about 2510 to 3040 g were divided in two groups: a control group and experimental group. The experimental group was divided into three subgroups for observation after 12, 24 and 48 hours of the operation, that consisted on a 4-0 polypropylene circular suture at 8 cm from the distal part of the cecal appendix. The control group was sham operated. The macroscopic exam (increase of the appendix volume, necrosis, perfuration, adherence and secretion in the abdominal cavity) and the microscopic finding showed a progression in the anatomopathological alterations. There was a close relationship between the histopathological findings and time after the appendiceal obstruction. We conclude that the method causes acute appendicitis and that the anathomo pathological alterations depends on the time elapsed between the operation and the postoperation findings.

[Cystadenoma of the pancreas. Various aspects of the diagnosis and surgical management adopted in 3 cases]. / Cistoadenoma do pâncreas. Aspectos do diagnóstico e da conduta cirúrgica adotados em três casos.

The authors report three cases of cystadenoma of the pancreas. Two cases were serouscystadenoma and one case was mucouscystadenoma. The best diagnostic procedures were computed axial tomography and ultrasonography. Decisions regarding operation depend on three factors: the patient's general conditions, site of the tumor and hystologic pattern. In the first case the elderly patient had the tumor in the head of the pancreas which had led to biliary obstruction. To establish satisfactory biliary drainage a biliodigestive anastomosis was used. The other two cases were younger patients with large protruding abdominal mass in the epigastrium and mesogastrium by a tumor of the body and tail of the pancreas. In these cases we opted for body pancreatectomy and splenectomy. Since the serouscystadenoma doesn't have the malignant potential that the mucouscystadenoma has, the surgical procedure can be different from the surgical resection used for the treatment of pancreatic cystadenoma.