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To report a case of severe lactic acidosis and hypoglycemia due to acute metformin intoxication in a dog.A female neutered Rat Terrier was presented for an acute onset of seizure-like episodes, weakness, and vomiting approximately 14 hours after ingestion of 198 mg/kg of metformin. The dog was found to be laterally recumbent, paddling, and unresponsive shortly before presentation. On physical exam, the dog was in hypovolemic shock and hypothermic. Blood work revealed severe lactic acidosis and hypoglycemia. The dog was volume resuscitated with intravenous crystalloids and dextrose, followed by a continuous infusion of intravenous fluids and dextrose, as well as administration of isotonic sodium bicarbonate. Repeat blood work showed minimal improvement of the hyperlactatemia for 3 hours despite resolution of hypovolemia and hypoglycemia followed by gradual improvement over the next 9 hours of hospitalization. High performance liquid chromatography/tandem mass spectrometry analysis showed markedly increased plasma metformin concentrations at 3.9 μg/mL. The dog was discharged from the hospital within 24 hours and showed no recurrence of clinical signs one year following discharge.Metformin-associated lactic acidosis and hypoglycemia is a severe complication in human patients, but has not been reported in veterinary medicine. Aggressive treatment with supportive care including IV fluids and dextrose administration resulted in resolution of the clinical signs in this patient. Metformin toxicosis should be considered in dogs with severe hyperlactatemia and hypoglycemia of unknown etiology.
We analyzed changes in apparent diffusion coefficient (ADC) during the cardiac cycle of the brain using bulk-motion-compensated diffusion imaging. ADC changes during the cardiac cycle were predominantly caused by water molecule fluctuations due to brain pulsation rather than the bulk motion of the brain parenchyma.
Echocardiography is commonly used for assessing cardiac structure and function in various species including non-human primates. A few previous studies reported normal echocardiographic reference intervals of clinically healthy rhesus macaques under sedation. However, these studies were under-powered, and the techniques were not standardized. In addition, body weight, age, and sex matched reference intervals should be established as echocardiographic measurements are commonly influenced by these variables. The purpose of this study was to establish reference intervals for complete echocardiographic parameters based on a large cohort of clinically healthy rhesus macaques with wide ranges of weight and age distributions using allometric scaling.A total of 823 rhesus macaques (ages 6 months to 31 years old; body weights 1.4 to 22.6 kg) were enrolled. Of these rhesus macaques, 421 were males and 402 were females. They were assessed with a complete echocardiographic examination including structural and functional evaluation under sedation with ketamine hydrochloride. The reference intervals of the key echocardiographic parameters were indexed to weight, age, and sex by calculating the coefficients of the allometric eq. Y = aMb. On correlation matrix, body weight, age, sex, and heart rate were significantly correlated with various echocardiographic parameters and some of the parameters were strongly correlated with body weight and age. Multiple regression analysis revealed that heart rate and body weight statistically significantly predicted several echocardiographic parameters. Valve regurgitation including tricuspid, aortic, pulmonic, and mitral regurgitations without other cardiac structural and functional abnormalities are common in clinically healthy rhesus macaques under ketamine sedation.In this study, the reference intervals of echocardiographic parameters were established by performing complete echocardiographic examinations on a large number of clinical healthy rhesus macaques. In addition, allometric scaling was performed based on their weight, and further indexed to age and sex. These allometrically scaled reference intervals can be used to accurately evaluate echocardiographic data in rhesus macaques and diagnose structural and functional evidence of cardiac disease.
Abstract Clopidogrel is converted to its active metabolite by cytochrome P450 isoenzymes and irreversibly inhibits platelet activation by antagonizing the adenosine-diphosphate (ADP) receptor. It is frequently used in cats with hypertrophic cardiomyopathy (HCM) to prevent thromboembolic complications. However, significant interpatient variability of the response to clopidogrel therapy has been suspected. In this study, we assessed the impact of single nucleotide polymorphisms (SNPs) within ADP receptor ( P2RY1, P2RY12 ) and cytochrome P450 isoenzyme ( CYP2C41 ) genes on platelet inhibition by clopidogrel administration in cats with HCM. Forty-nine cats completed the study, and blood samples were obtained before and after clopidogrel therapy to assess the degree of platelet inhibition based on flow cytometry and whole blood platelet aggregometry. Plasma concentrations of clopidogrel metabolites were measured after the last dose of clopidogrel. Whole blood platelet aggregometry revealed a significant reduction of platelet inhibition by clopidogrel in cats with the P2RY1:A236G and the P2RY12:V34I variants. The association with the P2RY1:A236G variant and clopidogrel resistance remained significant after adjustment for multiple comparisons. This study demonstrated that a genetic polymorphism in the P2RY1 gene altered response to clopidogrel therapy and suggests that clinicians may consider alternative or additional thromboprophylactic therapy in cats with the P2RY:A236G variant.
Acute blunt aortic rupture occurs frequently at the aortic isthmus and emergency operation is usually required. A 33-year-old man was suffered with blunt traumatic thoracic aortic injury caused by traffic accident and emergency operation was performed due to hemodynamic instability. The patient was operated through 'L'-thoracotomy (upper part sternotomy and antero-lateral thoracotomy). Cardiopulmonary bypass was initiated with right femoral vein drainage and right femoral arterial return and converted to standard cardiopulmonary bypass with the ascending aorta return and right atrium appendage drainage when the discending aorta was re-ruptured. It stabilized the circulation of upper body, especially brain. The post-operative course was uneventful. The 'L'-thoracotomy can provide good operative exposure for the aortic isthmus and stabilize the circulation of the brain with standard cardiopulmonary bypass and clamping the descending aorta.
Abstract Objective To compare hemostatic variables performed on blood samples obtained from indwelling jugular catheters or direct venipuncture over a 72‐hour period. Design Prospective experimental study. Setting University research laboratory. Animals Five healthy neutered male purpose‐bred Beagle dogs. Interventions Each dog was sedated to facilitate placement of a long‐stay 20‐Ga polyurethane IV catheter into the jugular vein. Blood samples were obtained from the preplaced catheters at 4 time points corresponding to 0, 24, 48, and 72 hours relative to placement. Blood samples were also obtained by direct venipuncture of a peripheral vein using a 21‐Ga butterfly catheter and evacuated blood tubes at the same time points. Platelet count, platelet closure time, prothrombin time, activated partial thromboplastin time, fibrinogen, and kaolin‐activated thromboelastography were performed on these paired samples at each time point. The patency of the indwelling catheters was maintained by flushing every 6 hours with heparinized saline. Measurements and Main Results No significant differences were identified in any of the hemostatic variables obtained by either blood collection technique at any time point during the study ( P > 0.05). There was also no significant day‐to‐day variation in any catheter‐derived hemostatic variable obtained from individual dogs identified over the course of the study. Conclusions These data suggest that accurate hemostatic variables may be obtained using blood collected from indwelling jugular catheters, maintained with heparinized saline for at least 72 hours, in healthy dogs.
