Abstract
To determine the incidence, outcome, and risk factors for postattenuation neurological signs (PANS) and seizures after attenuation of single congenital portosystemic shunts (CPSS) in dogs. Retrospective cohort study. Dogs (N = 253) with single CPSS. Medical records of dogs treated by surgical attenuation of a single CPSS between February 2000 and July 2015 were reviewed for signalment and preoperative and postoperative clinical outcomes, including the occurrence of PANS. Univariable and multivariable binary logistic regression was used to assess risk factors for PANS and for seizures. Twenty-eight (11.1%) dogs developed PANS, including 12 (4.7%) dogs with seizures. Five (17.9%) dogs with PANS did not survive to discharge. Risk factors for PANS included the presence of hepatic encephalopathy (HE) immediately preoperatively (P = .038, odds ratio [OR] 2.704, CI 1.057-6.922) and increasing age (P < .001, OR 1.476, CI 1.223-1.780). Risk factors for seizures included the presence of HE immediately preoperatively (P = .048, OR 3.538, CI 1.013-12.363) and increasing age (P = .009, OR 1.364, CI 1.082-1.720). No association was found between the location of portosystemic shunts (extrahepatic and intrahepatic) and post-operative PANS (P = .532) or seizures (P = .620). Similarly, preemptive administration of levetiracetam did not influence the risk of PANS (P = .991) or seizures (P = .752). Preoperative HE and older age in dogs with a CPSS increased the odds of developing PANS and seizures in our population. Preemptive administration of levetiracetam did not protect dogs against the development of PANS or seizures. Surgical attenuation of a single CPSS should not be excessively delayed, and surgeons should stabilize the clinical signs of HE before surgery to prevent postoperative PANS and seizures.
Highlights
Medical records of dogs with a single Congenital Portosystemic Shunts (CPSS) surgically attenuated between February 2000 and July 2015 were reviewed for signalment, pre and post-operative clinical data, including the occurrence of Post Attenuation Neurological Signs (PANS)
The risk factors for PANS included the presence of hepatic encephalopathy (HE) immediately pre-operatively (p=0.038, odds ratio 2.704, confidence interval 1.057-6.922) and increasing age (p
The risk factors for seizures included the presence of HE immediately pre-operatively (p=0.048, odds ratio 3.538, confidence interval 1.013-12.363) and increasing age (p=0.009, odds ratio 1.364, confidence interval 1.082-1.720)
Summary
Post Attenuation Neurological Signs (PANS) are a complication of the surgical management of Congenital Portosystemic Shunts (CPSS) reported in up to 12% of dogs.[1,2,3,4,5,6,7] Signs vary from mild ataxia 2,8 to generalized seizure activity. 5,6,9 PANS is a well recognised complication in dogs, the underlying aetiology is unclear and may be linked to changes associated with hepatic encephalopathy (HE) prior to surgery.Dogs with CPSS often show signs of HE, a poorly understood syndrome of neurological signs caused by alterations of multiple factors including ammonia and false neurotransmitters.[10,11,12] In dogs with CPSS, ammonia and inflammatory mediators predict the presence of HE13 and indicators of inflammation reduce following successful CPSS attenuation.[14]. Post Attenuation Neurological Signs (PANS) are a complication of the surgical management of Congenital Portosystemic Shunts (CPSS) reported in up to 12% of dogs.[1,2,3,4,5,6,7] Signs vary from mild ataxia 2,8 to generalized seizure activity. HE may cause chronic alterations in the central nervous system[15,16,17,18,19] and there is direct evidence of astrocyte alterations in the brains of dogs with CPSS. 10,21 It is hypothesised that the central nervous system becomes adapted to an abnormal metabolic environment pre-operatively and a sudden change to this favours an excitatory state.[2] Alternatively, damage to the CNS as a result of chronic portosystemic shunting, coupled with a metabolic event post attenuation could result in PANS.[6]
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