Presumptive Cycad Toxicosis in a Dog. Clinical and Magnetic Resonance Imaging Findings: A Case Report.

Cases of cycad toxicosis have been described in dogs that have presented with gastrointestinal, hematologic, hepatic, neurological, and carcinogenic signs. This case report describes brain magnetic resonance imaging (MRI) lesions in a dog with gastrointestinal and neurological signs secondary to cycad toxicosis. A 5-year-old neutered female Jack Russell terrier presented with a 2-days history of gastroenteric signs, progressive generalized tremors, and altered mentation after possible ingestion of Cycad revoluta. Neurologic examinations revealed disorientation, a wide-based stance, severe spasticity of the four limbs, intention tremors, severe cerebellar ataxia, decreased postural reactions in all four limbs, and intermittent decreased menace response in both eyes-all of which are consistent with a multifocal intracranial disorder involving the forebrain and cerebellum. A brain MRI showed diffuse/ill-defined, intra-axial bilateral and symmetrical changes, predominantly affecting the white matter of the cerebral hemispheres, thalamus, hippocampus, and cerebellum. A presumptive diagnosis of toxic-metabolic encephalopathy was made. Medical management of the clinical signs was performed, and the dog was discharged 7 days after presentation with no neurological abnormalities. Two and 8 weeks later, complete blood count (CBC), chemistry, electrolytes, and 8 weeks later brain MRI were performed, revealing no abnormalities. To the best of the authors' knowledge, this is the first case report describing lesions detected by brain MRI secondary to cycad toxicosis as well as a complete resolution of brain lesions on a follow-up MRI 8 weeks later.

Comparison of acid-base and electrolyte changes following administration of 6% hydroxyethyl starch 130/0.42 in a saline and a polyionic solution in anaesthetized dogs.

OBJECTIVE: To evaluate the effects of a 6% hydroxyethyl starch (130/0.42) in either a buffered, electrolyte-balanced (HES-BAL) or saline (HES-SAL) carrier solution on electrolyte concentrations and acid-base parameters in healthy anaesthetized dogs. STUDY DESIGN: Prospective randomised clinical study. ANIMALS: A group of 40 client-owned dogs undergoing general anaesthesia for elective surgical procedures or diagnostic imaging. METHODS: During anaesthesia, dogs were intravenously administered 15 mL kg-1 of either HES-SAL (n = 20) or HES-BAL (n = 20) over 30-40 minutes. Jugular blood samples were analysed before (T0) and 5 minutes (T5), 1 hour (T60) and 3 hours (T180) after fluid administration. Sodium, potassium, chloride, ionised calcium, phosphate, albumin, pH, venous pCO2, base excess (BE), bicarbonate and anion gap were determined and strong ion difference (SID) and total quantity of weak nonvolatile acids were calculated for each time point. RESULTS: Chloride was significantly increased at T5, T60 and T180 compared with T0 after HES-SAL, and was significantly greater after HES-SAL than after HES-BAL at T5 (p = 0.042). Ionised calcium was significantly decreased at T5 compared with T0 after HES-SAL, and was significantly lower after HES-SAL than after HES-BAL at T5 (p < 0.001). Bicarbonate was significantly lower after HES-SAL than after HES-BAL at T5 (p = 0.004) and T60 (p = 0.032). BE was significantly lower after HES-SAL than after HES-BAL at T5 (p < 0.001) and T60 (p = 0.007). SID was significantly decreased after HES-SAL at T5 and T60 compared with T0, and was significantly lower after HES-SAL than after HES-BAL at T5 (p = 0.027). Mean electrolyte and acid-base parameters remained within or marginally outside of reference intervals. CONCLUSIONS AND CLINICAL RELEVANCE: Changes in both groups were minor and short-lived with either fluid in healthy individuals, but might become clinically relevant with higher fluid doses or in critically ill dogs.

Red blood cell storage lesion.

OBJECTIVE: To summarize current understanding of the mechanisms responsible for changes occurring during red blood cell (RBC) storage, collectively known as the storage lesion, and to review the biological and clinical consequences of increasing storage time of RBCs. DATA SOURCES: Human and veterinary clinical studies, experimental animal model studies, and reviews of the RBC storage lesion with no date restrictions. HUMAN DATA SYNTHESIS: Experimental studies have characterized the evolution of human RBC and supernatant changes that occur during storage and form the basis for concern about the potential for harm from long-term storage of RBCs. Although 4 randomized controlled trials of varying sizes failed to find an association between RBC storage time and negative clinical outcomes, a recent meta-analysis and numerous observational clinical studies have demonstrated that transfusion of old versus fresh stored RBCs is associated with an increased risk of morbidity and mortality, particularly among trauma victims and cardiac surgery patients. Potential clinical consequences of RBC transfusion following development of the storage lesion include risk of organ dysfunction, organ failure, infections, and death. VETERINARY DATA SYNTHESIS: Experimental animal models have contributed to the evidence supporting adverse consequences of the RBC storage lesion. Studies on relevant RBC storage issues such as the effect of different preservative solutions and leukoreduction have been completed. Transfusion with RBCs stored for 42 days increases mortality in dogs with experimental sepsis. CONCLUSION: Storage of RBCs induces progressive biochemical, biomechanical, and immunologic changes that affect red cell viability, deformability, oxygen carrying capacity, microcirculatory flow, and recipient response. Most reports in the human and veterinary literature support the concept that there are deleterious effects of the RBC storage lesion, but additional studies with improved experimental design are needed to identify compelling reasons to modify current blood banking and transfusion practices.