ABSTRACT
CASE SERIES SUMMARY: The objective of this case series was to describe the presentation, surgical treatment and outcome of a congenital intrahepatic portosystemic shunt (IHPSS) in 12 cats. A retrospective case series of cats undergoing surgical treatment for an IHPSS was undertaken. Signalment, clinical signs, imaging, surgical treatment, complications and short-term outcome (<30 days) were obtained using medical records. Long-term outcome (>1 year after first surgery) was obtained, where possible, using a health-related quality of life owner questionnaire. Seven cats were diagnosed with a left divisional shunt, three with a central divisional shunt and two with a right divisional shunt using intraoperative mesenteric portovenography. Three cats tolerated complete acute suture attenuation, eight cats underwent partial suture attenuation, four of which received complete suture ligation at a second surgery, and one cat underwent partial attenuation with a thin film band. Six cats (50%) developed post-attenuation neurological signs (PANS) after first surgery and two cats (17%) died or were euthanased due to severe PANS. Long-term outcome was available for eight cats (67%), with a median follow-up time of 1743 days (range 364-2228), and was described as excellent in five cats (63%), fair in two cats (25%) and poor in one cat (12%). RELEVANCE AND NOVEL INFORMATION: Few papers exist that describe the presentation, intraoperative imaging, treatment and outcome of IHPSSs in cats. This is the first to describe surgical attenuation with a thin film band in a cat with an IHPSS. This case series reports excellent long-term outcomes in a majority of surgically treated cats with IHPSS.
Subject(s)
Cat Diseases , Portal System , Animals , Cat Diseases/diagnostic imaging , Cat Diseases/surgery , Cats , Portal System/abnormalities , Postoperative Complications/veterinary , Quality of Life , Retrospective Studies , Treatment OutcomeABSTRACT
C-type natriuretic peptide (CNP) is the major natriuretic peptide of the central nervous system and acts via its selective guanylyl cyclase-B (GC-B) receptor to regulate cGMP production in neurons, astrocytes and endothelial cells. CNP is implicated in the regulation of neurogenesis, axonal bifurcation, as well as learning and memory. Several neurological disorders result in toxic concentrations of ammonia (hyperammonaemia), which can adversely affect astrocyte function. However, the relationship between CNP and hyperammonaemia is poorly understood. Here, we examine the molecular and pharmacological control of CNP in rat C6 glioma cells and rat GPNT brain endothelial cells, under conditions of hyperammonaemia. Concentration-dependent inhibition of C6 glioma cell proliferation by hyperammonaemia was unaffected by CNP co-treatment. Furthermore, hyperammonaemia pre-treatment (for 1 h and 24 h) caused a significant inhibition in subsequent CNP-stimulated cGMP accumulation in both C6 and GPNT cells, whereas nitric-oxide-dependent cGMP accumulation was not affected. CNP-stimulated cGMP efflux from C6 glioma cells was significantly reduced under conditions of hyperammonaemia, potentially via a mechanism involving changed in phosphodiesterase expression. Hyperammonaemia-stimulated ROS production was unaffected by CNP but enhanced by a nitric oxide donor in C6 cells. Extracellular vesicle production from C6 cells was enhanced by hyperammonaemia, and these vesicles caused impaired CNP-stimulated cGMP signalling in GPNT cells. Collectively, these data demonstrate functional interaction between CNP signalling and hyperammonaemia in C6 glioma and GPNT cells, but the exact mechanisms remain to be established.
Subject(s)
Cyclic GMP/metabolism , Endothelial Cells/metabolism , Glioma/metabolism , Hyperammonemia/metabolism , Animals , Brain/metabolism , Natriuretic Peptide, C-Type/metabolism , Natriuretic Peptides/metabolism , Phosphoric Diester Hydrolases/metabolism , Rats , Signal Transduction/drug effectsABSTRACT
PRACTICAL RELEVANCE: Traumatic joint luxations are usually associated with significant trauma and there may be concomitant systemic injury. Joints are unstable as a result of injury to one or more supporting structures and the clinician should aim to determine which structures are damaged with physical examination, diagnostic imaging and careful assessment under sedation/anaesthesia. The aim is to reduce the joint back to its anatomical position, and then to maintain this through repair of damaged structures. However, where this is not possible, replacement or removal (arthrodesis/excision arthroplasty) of the joint remain viable options. CLINICAL CHALLENGES: Owing to the small size of feline joints and the severity of damage often seen, surgical management of these cases can be challenging. The first priority is to ensure the patient is systemically well before embarking on any specific surgical treatment of a luxated joint. Cats also present challenges in the postoperative period and a lack of patient and owner compliance can be detrimental to postoperative outcomes. AIMS: This article aims to help the reader diagnose joint luxations and to assist decision-making with an overview of the management and treatment options available. EVIDENCE BASE: There are a number of original articles and textbook chapters in the literature covering aspects of different joint luxations, particularly for the more common luxations. This article draws on information from key feline research and, where necessary, extrapolates from relevant canine research. The authors also offer practical guidance based on their own clinical experience.
Subject(s)
Cat Diseases/surgery , Joint Dislocations/veterinary , Wounds and Injuries/veterinary , Animals , Arthrodesis/veterinary , Cats , Joint Dislocations/surgery , Wounds and Injuries/surgeryABSTRACT
OBJECTIVE: To determine the incidence, outcome, and risk factors for postattenuation neurological signs (PANS) in cats treated for single congenital portosystemic shunts (CPSS). STUDY DESIGN: Retrospective cohort study. ANIMALS: Cats (n = 50) with a single CPSS. METHODS: Medical records of cats treated by surgical attenuation of a single CPSS between 2003 and 2017 were reviewed for signalment, surgical technique, preoperative management and postoperative clinical outcomes. Binary logistic regression was performed to investigate risk factors for occurrence of PANS and seizures. RESULTS: Congenital portosystemic shunts in 50 cats included 40 extrahepatic and 10 intrahepatic shunts. Postattenuation neurological signs were recorded in 31 (62%) cats and graded as 1 in 10 cats, 2 in nine cats, and 3 in 12 cats. Postattenuation neurological signs included seizures in 11 cats. Five of 31 cats with PANS did not survive to discharge. No association was detected between PANS or seizures and the type of CPSS (intrahepatic or extrahepatic), degree of attenuation, age, or the use of perioperative levetiracetam or hepatic encephalopathy immediately preoperatively. Osmolality at a median 24 hours postoperatively was lower in cats with PANS (P < .049, Wald 3.867, odds ratio [Exp(B)] 0.855, CI 0.732-0.999). CONCLUSION: Postattenuation neurological signs are common complications in cats treated for CPSS. Preoperative levetiracetam did not prevent the occurrence of PANS or seizures. The only risk factor for PANS detected was lower postoperative Osmolality in cats with PANS at 24 hours. CLINICAL SIGNIFICANCE: Postattenuation neurological signs including seizures occur frequently in cats undergoing surgical attenuation of a CPSS. Preoperative levetiracetam did not protect against the development of PANS.
Subject(s)
Cats/surgery , Portal System/abnormalities , Postoperative Complications/veterinary , Seizures/veterinary , Vascular Malformations/veterinary , Animals , Cats/abnormalities , Cohort Studies , Female , Incidence , Male , Postoperative Complications/epidemiology , Postoperative Complications/etiology , Retrospective Studies , Risk Factors , Vascular Malformations/surgeryABSTRACT
OBJECTIVE: 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. STUDY DESIGN: Retrospective cohort study. SAMPLE POPULATION: Dogs (N = 253) with single CPSS. METHODS: 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. RESULTS: 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). CONCLUSION: 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. CLINICAL SIGNIFICANCE: 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.