COMBINED USE OF ULTRASONOGRAPHY AND CONTRAST ENHANCED COMPUTED TOMOGRAPHY TO EVALUATE ACUTE NECROTIZING PANCREATITIS IN TWO DOGS

The imaging findings in two miniature schnauzers with acute necrotizing pancreatitis are described. Both dogs were treated previously for diabetes mellitus and hyperlipidemia. Vomiting, anorexia, and lethargy were observed in both dogs at presentation. Laboratory evaluations supportive of pancreatitis included left shift, abnormally high serum amylase and lipase activities, hypocalcemia, and abnormally high serum activities of liver enzymes. Sonographically, both dogs had diffusely enlarged hypoechoic pancreatic tissue with anechoic foci compatible with necrosis, abscessation, phlegmon, and pseudocysts formation. Contrast-enhanced computed tomography (CT) findings in both dogs were compatible with pancreatic necrosis. Dog 1 was managed medically for 11 days. Follow-up CT scan in this dog disclosed decreased pancreatic size and increased contrast enhancement compatible with partial resolution of pancreatitis.     

INADVERTENT INTRATHECAL ADMINISTRATION OF DIATRIZOATE MEGLUMINE AND DIATRIZOATE SODIUM DURING MYELOGRAPHY IN A DOG

A dog undergoing diagnostic myelography inadvertently received 0.5 ml diatrizoate meglumine (66%) and (10%) diatrizoate sodium via intrathecal injection. This resulted in post-operative seizures requiring extended sedation of the patient. The clinical course and management of this patient are presented. Complications associated with the inappropriate administration of a hyperosmolar contrast agent into the subarachnoid space and the results of similar accidents in humans are also discussed. The dog in the report recovered with no evidence of long trem neurological dam     

Influence of Cholinergic Blockade on the Development of Epinephrine-Induced Ventricular Arrhythmias in Halothane- and Isoflurane-Anesthetized Dogs

The arrhythmogenic effects of anesthetic drugs are assessed using the arrhythmogenic dose of epinephrine (ADE) model. The purpose of this study was to determine the influence of cholinergic blockade (CB) produced by glycopyrrolate (G) on ADE in 1.5 minimum alveolar concentration (MAC) halothane (H)- and isoflurane (I)-anesthetized dogs. Eight dogs (weighing between 12.5 and 21.5 kg) were randomly assigned to four treatment groups (H, HG, I, and IG) and each treatment was replicated three times. Anesthesia was induced and maintained with H (1.31%, end-tidal [ET]) or I (1.95%, ET) in oxygen. Ventilation was controlled (carbon dioxide [PCO₂] 35 to 40 mmHg, ET). G was administered 10 minutes before ADE determination at a dose of 22 μg/kg (11 μg/kg, intravenous [IV] and 11 μg/kg, intramuscular [IM]). The ADE was determined by IV infusion of epinephrine at sequentially increasing rates of 1.0, 2.5, and 5.0 μg/kg/min; and defined as the total dose of epinephrine producing at least four ectopic ventricular contractions (EVCs) within 15 seconds during a 3-minute infusion and up to 1 minute after the end of the infusion. Total dose was calculated as the product of infusion rate and time to arrhythmia. Data were analyzed using a randomized complete block analysis of variance. When significant (P < .05) F values were found a least significant difference test was used to compare group means. Values are reported as means ± standard error. The ADE (μg/kg) for H, HG, I, and IG were 1.53 ± 0.08, 3.37 ± 0.46, 1.61 ± 0.21, and > 15.00, respectively. Heart rates (HRs) (beats/min) and systolic pressures (mmHg) at the time of arrhythmia formation for H, HG, I, and IG were (60.3 ±4.0 and 142.0 ± 7.6), (213.0 ± 13.1 and 239.2 ± 7.1), (62.9 ± 4.5 and 151.9 ± 6.3), and (226.3 ± 6.1 and 323.5 ± 3.4), respectively. The H and I ADE were not different. The HG ADE was significantly less than the IG ADE. The H and I ADE were significantly less than the HG and IG ADE. We conclude the following from the results of this study of epinephrine infusion in halothane- and isoflurane-anesthetized dogs: (1) two distinct mechanisms are responsible for the development of arrhythmias, (2) CB produced by G significantly increases ADE but is associated with higher rate pressure products (RPP) and myocardial work, and (3) ADE methodology could be improved by determining ADE with and without CB.     

Effects of Halothane, Enflurane, and Isoflurane on Supraventricular and Ventricular Rate in Dogs With Complete Atrioventricular Block

Complete atrioventricular (AV) block was produced in 32 chloralose-anesthetized autonomically intact dogs to determine the effects of halothane, enflurane, and isoflurane on supraventricular and ventricular rate. Halothane (n = 17), enflurane (n = 6), and isoflurane (n = 9) were administered in three separate experiments in sequential minimum alveolar concentration (MAC) multiples of 0.5, 1.0, 1.5, 2.0, 1.5, and 1.0. Supraventricular rate, ventricular rate, and mean arterial blood pressure (MAP) were measured and recorded at baseline and after a 20-minute equilibration period of each inhalation anesthetic at each MAC multiple. Increasing concentrations of enflurane and isoflurane significantly decreased supraventricular rate ( P < .05). Ventricular rate was not significantly changed by sequential MAC multiples of halothane, enflurane, and isoflurane. Increasing concentrations of halothane, enflurane, and isoflurane significantly decreased MAP with enflurane producing the most significant decrease ( P < .05). Ventricular arrhythmias occurred in 5 of 17 dogs anesthetized with halothane and 1 of 9 dogs anesthetized with isoflurane. Inhalation anesthesia can significantly decrease supraventricular rate and MAP, does not alter ventricular rate, and can produce ventricular arrhythmias in dogs with complete AV block.     

Brown recluse spider (Loxosceles reclusa) envenomation in small animals

Objective – To provide a comprehensive review of relevant literature regarding the brown recluse spider (BRS) and to define those criteria that must be satisfied before making a diagnosis of brown recluse envenomation.
Etiology – The complex venom of the BRS contains sphingomyelinase D, which is capable of producing all the clinical signs in the human and some animal models.
Diagnosis – There is no current commercially available test. In humans there are many proposed guidelines to achieve a definitive diagnosis; however, there are no established guidelines for veterinary patients.
Therapy – Currently, no consensus exists for treatment of BRS envenomation other than supportive care, which includes rest, thorough cleaning of the site, ice, compression, and elevation.
Prognosis – Prognosis varies based on severity of clinical signs and response to supportive care.     

Potential Iatrogenic Medial Meniscal Damage During Tibial Plateau Leveling Osteotomy

Objective— To evaluate potential iatrogenic medial meniscal (MM) damage during tibial plateau leveling osteotomy (TPLO) and to establish a safe zone (SZ) for hypodermic needle (HN) identification of the medial aspect of the stifle joint.
Study Design— Prospective cohort.
Animals— Cadaveric canine stifles (n=40).
Methods— HN (20 or 25 G) were inserted through the medial collateral ligament (MCL) of the femorotibial joint and through the SZ insertion points. The medial meniscus was inspected for iatrogenic damage. Statistical comparison of MM damage caused by different needle sizes and insertion sites was performed using Fisher's exact test with significance at P <.05.
Results— Twenty-gauge group: 65% of stifles had minor MM damage with MCL insertion compared with 35% of stifles with SZ insertion ( P =.0049). Severe MM damage occurred in 25% of stifles with MCL insertion compared with 0% of stifles with SZ insertion ( P =.0014). Twenty-five-gauge group: 85% of stifles had minor MM damage with MCL insertion compared with 30% after SZ insertion ( P =.0011); however, no severe MM injury was noted.
Conclusions— HN insertion though the MCL can produce iatrogenic damage to the MM. Use of a 25 G HN and SZ site for insertion reduced the frequency and severity of MM damage.
Clinical Relevance— HN insertion into the medial aspect of the femorotibial joint during TPLO can cause gross iatrogenic MM damage, which may contribute to the incidence and misdiagnosis of latent MM injuries after TPLO.