Spinal cord dysfunction secondary to spinal arachnoid diverticula (SAD) has been widely reported in the veterinary literature and there is some suggestion that surgical treatment may provide better outcomes than medical treatment. Despite this, previous reports have mentioned cases with recurrence of clinical signs following surgical treatment but the cause for this has not been further investigated. The medical records of seven dogs and one cat which presented for investigation of recurrence of neurological deficits at least six months after surgery for SAD were retrospectively reviewed. Median time to relapse of the neurological deficits was 20.5 months after surgery. On repeated imaging, 3/8 cases showed clear regrowth of diverticulum, 2/8 cases showed dorsal compression at the previous laminectomy site (presumed to be the laminectomy membrane), and 3/8 cases showed herniation of the spinal cord through the laminectomy defect associated with a stellate appearance to the spinal cord with small multiloculated areas of dilation of the subarachnoid space. Repeat surgical intervention was most successful in the cases where SAD recurrence was identified while medical treatment resulted in either subtle improvement or stabilisation on the clinical signs, sometimes followed by slow deterioration.
Background: Urinary (UI) and fecal (FI) incontinence occur in up to 7.5% and 32% of dogs, respectively, after thoracolumbar acute noncompressive nucleus pulposus extrusion (ANNPE).Hypotheses/Objectives: To investigate clinical, diagnostic, and therapeutic predictors of UI and FI in dogs with ANNPE affecting the T3-L3 spinal cord segments.Animals: Hundred and eighty-seven dogs with T3-L3 ANNPE diagnosed based on clinical and MRI findings.Methods: Multicenter retrospective study. Data were obtained from medical records and telephone questionnaires and analyzed by logistic regression.Results: UI and FI were reported in 17 (9.1%) and 44 (23.5%) dogs, respectively. Paraplegic dogs were 3 times (95% CI = 1.25, 10.87) more likely to develop UI (P = .018) and 4 times (95% CI = 1.94, 12.56) more likely to develop FI (P = .001) compared to nonparaplegic dogs. Dogs with an intramedullary hyperintensity greater than 40% of the cross-sectional area of the spinal cord at the same level on transverse T2-weighted MRI images were 4 times more likely to develop UI (95% CI = 1.04, 21.72; P = .045) and FI (95% CI = 1.56, 10.39; P = .004) compared to dogs with smaller lesions. FI was 3 times (95% CI = 1.41, 7.93) more likely in dogs that were not treated with nonsteroidal anti-inflammatory drugs (NSAIDs) after diagnosis compared to dogs administered NSAIDs (P = .006) and 2 times (95% CI = 1.12, 5.98) more likely in dogs presented with clinical signs compatible with spinal shock compared to dogs without (P = .026).Abbreviations: ANNPE, acute non-compressive nucleus pulposus extrusion; COX2, cyclooxygenase-2; FI, fecal incontinence; LL:VL, ratio of the length of the intramedullary lesion to the length of the L2 vertebra; NSAIDs, nonsteroidal anti-inflammatory drugs;PCSAL, percentage of the cross-sectional spinal cord area occupied by the lesion; SCI, spinal cord injury; UI, urinary incontinence.
Background Status epilepticus (SE) is an emergency associated with serious consequences for both patient and owner. Data regarding risk factors for short‐term mortality or recurrence in dogs with SE is limited. Objective Identify risk factors associated with short‐term mortality (euthanasia or spontaneous death) and recurrence of SE in dogs. Animals One hundred twenty‐four client‐owned dogs that sustained an episode of SE. Methods Retrospective multicenter study using data collected from medical records of dogs presented in SE to the contributing institutions. Multivariable logistic regression analysis was performed using a manual backwards stepwise approach to identify risk factors associated with short‐term mortality and recurrence of SE after discharge. Results Short‐term mortality for affected dogs was 29.8%. Factors significantly associated with short‐term mortality included increased patient age, shorter duration of hospitalization, development of SE before arrival, and SE caused by a potentially fatal etiology. Status epilepticus recurred in 27% of dogs that survived to discharge. Factors significantly associated with recurrence of SE included prior history of pharmacoresistant epilepsy and predominance of a focal seizure phenotype. Conclusions and Clinical Importance Our results may be used to inform clinicians and dog owners regarding risk factors for both short‐term mortality and recurrence in dogs with SE.
A 1-year-old, female intact Pug dog was presented to the Small Animal Teaching Hospital of the University of Liverpool with a 4-week history of progressive multifocal intracranial signs. Magnetic resonance imaging (MRI) detected multiple hemorrhagic lesions in the brain. The Baermann and zinc sulfate flotation tests with centrifugation, performed on fecal samples, were positive for lungworm larvae and an antigenic test confirmed Angiostrongylus vasorum infection. Anthelmintic treatment was started with a consequent marked clinical improvement. Seventy days later, the dog was clinically normal, and no larvae were detected on the Baermann test. Repeat MRI of the brain revealed marked improvement of the hemorrhagic lesions. Cerebrospinal fluid analysis (CSF) showed marked eosinophilic pleocytosis, and anthelmintic treatment was restarted. A follow-up CSF analysis 4 months after the first presentation revealed resolution of the eosinophilic pleocytosis. This is the first case report of marked eosinophilic pleocytosis associated with neural A vasorum infection in a dog. The CSF eosinophilic pleocytosis persisted for several weeks after treatment, even in the absence of concurrent clinical signs and with a negative A vasorum Baermann test. K E Y W O R D S brain hemorrhage, canine angiostrongylosis, central nervous system, CSF, eosinophils, larval migration 1 | CASE PRESENTATION A 1-year-old female intact Pug dog was referred to the Neurology Service at the Small Animal Teaching Hospital (SATH), the University of Liverpool, for investigation of progressive truncal swaying, ataxia, right-sided head tilt, altered mentation, right eye exophthalmia, and conjunctival hyperemia. Clinical signs started 4 weeks prior to referral. The dog had always lived in the United Kingdom (UK), had never traveled abroad, and the vaccination status was up to date; however, no ectoparasite or endoparasite (including lungworm) prevention was given. The dog had free access to the outdoors where the dog could encounter wild animals. A CBC (LaserCyte Dx; IDEXX Laboratories,Westbrook, ME, USA) performed 6 days prior to referral revealed a mild leukocytosis (18.64 × 10 9 /L; RI 5.50-16.90) due to a mild neutrophilia (12.92 × 10 9 /L; RI 2-12) and mild monocytosis (3.16 × 10 9 / L; RI 0.30-2.00). Basophils were minimally increased (0.11 × 10 9 /L; RI 0.00-0.10), but the blood smear was not reviewed. The serum biochemistry profile (Catalyst Dx; IDEXX Laboratories) revealed mildly increased urea (12.4 mmol/L; RI 2.5-9.6), marginally increased ALP (227 IU/L; 23-212), and moderate hyperproteinemia (93 g/L; 52-82) due to moderate hyperglobulinemia (63 g/L; 25-45).Abstract presented in the 31st Annual Symposium of the ESVN-ECVN,
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