Epidural Morphine in Goats after Hindlimb Orthopedic Surgery

Morphine (0.1 mg/kg) diluted with 0.9% saline to a volume of 0.13 mL/kg was administered into the epidural space at the lumbosacral junction in 10 halothane-anesthetized goats immediately before discontinuation of halothane. The same volume of 0.9% saline was given to control group of eight anesthetized goats. Both groups had undergone an orthopedic procedure that replaced the anterior cruciate ligament with a patellar tendon autograft. The appearance and unprovoked behavior of goats in the morphine group were significantly different (p < .05) from the saline groups. The goats in the morphine group were more sedate and struggled less during recovery. Epidural morphine did not produce respiratory depression or bloat during a 9 hour observation period. Heart rate, respiratory rate, and blood pressure (mean, systolic, and diastolic) of the morphine group did not differ from those of the control group.     

Parenteral Anticholinergics in Dogs With Normal and Elevated Intraocular Pressure

Dogs given parenteral anticholinergic drugs have been thought to be at risk for development or exacerbation of elevated intraocular pressure (IOP). In a randomized, blinded, placebo-controlled study, we evaluated the effect of intramuscular glycopyrrolate (0.01 mg/kg) on pupil diameter and IOP in unanesthetized normal dogs. Treatment with glycopyrrolate did not change pupil diameter or IOP from baseline, nor were there differences between glycopyrrolate and saline-treated (control) dogs. In addition, the authors retrospectively reviewed the medical records of 2,828 dogs undergoing general anesthesia between April 1987 and September 1990 to determine if there was an association between parenteral anticholinergic medication and postanesthetic elevation in IOP. The authors also determined the frequency of bradycardia requiring anticholinergic therapy during anesthesia in dogs with glaucoma. Of the 2,828 cases reviewed, the records of 46 dogs coded for glaucoma were examined in detail. The 46 dogs underwent 62 episodes of anesthesia, with 23 episodes including exposure to an anticholinergic drug. An increase in IOP from preanesthetic to postanesthetic measurement occurred in three dogs. One of these dogs received anticholinergic medication for bradycardia during anesthesia. The postanesthetic elevation in IOP in this dog was probably not drug related. Preanesthetic anticholinergic administration did not affect the incidence of anticholinergic administration for bradycardia during the anesthetic episode. Anticholinergic therapy during anesthesia was more frequent when the preanesthetic medication included an opiate drug. These studies do not indicate an association between parenteral anticholinergic administration and elevations in IOP.     

Pharyngeal Mucoceles in Dogs

Eight cases of pharyngeal mucoceles were diagnosed in 49 dogs with salivary mucoceles over a 7 year period. Five of the eight pharyngeal mucoceles were seen in Miniature Poodles. The presenting complaint in all eight dogs was labored breathing, with or without coughing upon excitement or exercise. Diagnosis was made by aspirating a thick mucoid fluid from the pharyngeal swelling. Treatment consisted of resection of the mandibular and sublingual salivary glands on the affected side and aspiration of the mucocele in all eight dogs, and resection of redundant pharyngeal tissue in five dogs. Time to follow-up ranged from 1.5 to 7.5 years. There were no postsurgical complications or recurrences of the mucocele.     

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.     

Physeal Fractures in the Horse II. Management and Outcome

Seventy physeal fractures in horses were initially managed by euthanasia (18), stall confinement (25), application of a cast (7), or internal fixation (20). Of the 52 physeal fractures initially managed with stall confinement, a cast, or internal fixation, 23 (44%) healed and 13 (25%) of these horses became sound. The number of horses less than 4.5 months of age with pressure physeal fractures that became sound was significantly higher (p < 0.05) than the number of horses greater than 4.5 months of age. The number of horses with functional, pain-free limbs (sound horses) or functional limbs (lame horses) was not significantly different (p > 0.05) for Salter-Harris Type I, II, III, or IV pressure physeal fractures; however, critical examination for growth disturbances was not performed. The number of horses with pressure or traction physeal fractures of less than 5 days duration prior to presentation that healed or became sound was not significantly different (p > 0.05) when compared with those horses with fractures of greater than or equal to 5 days duration.     

Evaluation of an Omental Pedicle Extension Technique in the Dog

A two-step omental pedicle extension technique was performed on 10 dogs. Step 1 of the pedicle extension involved release of the dorsal leaf of the omentum from its pancreatic attachment, whereas step 2 consisted of an inverse L-shaped incision to double the length of the pedicle. The pedicle dimensions were measured and the distance reached when extended toward the hind limb, forelimb, and the muzzle recorded after each stage of the procedure. The vascular patency of the pedicle was determined by intravenous injection of flu-orescein dye after the second stage of omental extension. Mean pedicle lengths were 44.5 cm with the first stage of extension and 82.0 cm after full extension. The mean width at the caudal extent of the pedicles after dorsal and full extension was 30.4 cm and 17.2 cm, respectively. Eight of the 10 pedicles were patent after full extension. The fully extended omental pedicles reached and, in most cases, extended beyond the distal extremities and the muzzle. The findings in this study suggest that the canine omentum can be extended to any part of the body without being detached from its vascular supply.     

Morphologic Effects of Experimental Distention of Equine Small Intestine

The morphologic effects of induced intraluminal hydrostatic pressures (IHPs) of 0, 9, and 18 cm H₂O were evaluated in 33 isolated equine jejunal segments. Fifteen segments were distended with Tyrode's solution for 1 hour and nine segments for 4 hours. Tyrode's solution was added as needed to maintain the prescribed pressures. Nine other segments were left undisturbed for 4 hours after the initial distention period. On decompression of the intestinal segments, progressive peristaltic contractions resumed in all segments. Evaluation of intestinal sections by light microscopy and transmission electron microscopy showed edema of the villi and submucosa and separation of the epithelial cells adjacent to the basement membrane in all segments. The epithelial cell necrosis found in ischemic intestine was not seen. This study indicates that the necrosis found at the villous tips in distended sections of small intestine remote from the site of obstruction cannot be reproduced by IHP increases of 4 hours duration.     

Attempts to Modify Reperfusion Injury of Equine Jejunal Mucosa Using Dimethylsulfoxide, Allopurinol, and Intraluminal Oxygen

This study compared the severity of ischemic injury to the equine jejunal mucosa caused by arteriovenous obstruction (AVO) or venous obstruction (VO) with that caused by reperfusion after ischemia. The degree of mucosal damage and regeneration was scored according to a modified version of an established light microscopic classification for ischemic injury. Biopsy specimens taken after 3 and 4 hours of obstruction, and after 3 hours of obstruction and 1 hour of reperfusion, were compared. There were no changes in the severity of mucosal injury (characterized by epithelial sloughing, loss of villus architecture, and necrosis of crypt cells) at 4 hours of ischemia when compared with 3 hours of ischemia. The mucosal injury score increased by one grade in three of six and five of eight segments during reperfusion for the VO and AVO models, respectively; however, only the scores for the AVO model were significantly different from the injury caused by ischemia alone. Modification of reperfusion injury was attempted by the administration of intravenous (IV) allopurinol, dimethyl sulfoxide (DMSO), or intraluminal oxygen insufflation at the time of release of the AVO and VO. Treatments did not significantly alter either the severity of injury noted after 1 hour of reperfusion or the degree of mucosal regeneration after 48 hours of reperfusion. In this group of ponies, the severity of mucosal damage was greater after 1 hour of reperfusion for both AVO and VO.     

Hepatic Lobe Torsion as a Cause of Colic in a Horse

A 14-year-old Arabian gelding was examined for colic. An exploratory celiotomy was subsequently performed and the left lobe of the liver was found to be twisted. The lobe was resected using a TA-90 surgical stapling instrument. Histologic examination of the resected liver indicated portal vein and sinusoid dilation and congestion with blood. There were focal areas of necrosis and bacterial cocci and rods throughout the section. The histologic findings were consistent with hepatic lobe torsion. After surgery, the horse was treated with broad spectrum antibiotics, anti-inflammatory drugs, heparin, and intravenous fluids. The horse recovered without complications, although serum liver enzymes remained elevated for more than 1 week after surgery. Seven months after surgery the horse showed no adverse affects from the disease.     

Effects of Thiopental, Ketamine, Diazepam, Xylazine, and Nitrous Oxide on EEG Spike Activity and Convulsive Behavior During Enflurane Anesthesia in Atropinized Cats Effect of Increasing Inhalant Concentrations

The effects of thiopental, ketamine, diazepam, xylazine, and nitrous oxide, and the combinations of thiopental-nitrous oxide and ketamine-nitrous oxide, on both enflurane-induced electroencephalographic (EEG) spike activity and convulsive behavior were measured quantitatively in atropinized cats receiving enflurane with controlled ventilation. Pretreatments with thiopental, ketamine, and diazepam reduced both EEG spike frequency and amplitude at 2.5% to 4.5% inspired enflurane but did not abolish spike activity. Nitrous oxide (66% of inspired gas) did not significantly alter spike frequency or amplitude during 2.5% to 4.5% inspired enflurane, but the combination of thiopental-nitrous oxide or ketamine-nitrous oxide reduced EEG spike activity during 2.5% inspired enflurane. Enflurane-induced convulsive score was markedly suppressed by thiopental and ketamine and was significantly reduced by diazepam, xylazine and nitrous oxide. The combinations of thiopental-nitrous oxide and ketamine-nitrous oxide greatly reduced behavioral-convulsive responses induced by 2.5% to 4.5% inspired enflurane.