A search for and the development of more objective and reliable methods of lameness evaluation is justified and should be encouraged and supported.
The inertial sensor system was able to identify lameness at a lower level of sole pressure than the consensus of 3 equine veterinarians. The inertial sensor system may be an effective aid to lameness localisation in clinical cases.
Although much has been written about laminitis in the context of its association with inflammatory processes, such as dietary carbohydrate overload and endotoxemia, [1][2][3][4][5] recognition is growing that most cases of laminitis examined by veterinarians in private practice are those associated with pasture grazing, obesity, and insulin resistance (IR). 6,7 The term endocrinopathic laminitis has been adopted to classify the instances of laminitis in which the origin seems to be more strongly associated with an underlying endocrinopathy, such as either IR or the influence of corticosteroids. [8][9][10][11] Results of a recent study suggest that obesity and IR represent the most common metabolic and endocrinopathic predispositions for laminitis in horses. 6,12 IR also plays an important role in the pathogenesis of laminitis that develops when some horses or ponies are allowed to graze pastures at certain times of the year (pasture-associated laminitis [PAL]). [12][13][14][15] Moreover, IR is provoked by and contributes to pathophysiologic processes associated with endotoxemia and systemic inflammation under the more classic circumstances associated with risk for acute laminitis, such as grain overload, retention of fetal membranes, and gastroenteritis. 16,17 However, a recent study using the oligofructose model showed that experimentally induced laminitis was not associated with a loss of insulin sensitivity. 18 The term equine metabolic syndrome (EMS) has been proposed as a label for horses whose clinical examination results (including both physical examination and laboratory testing) suggest heightened risk for developing laminitis as a result of underlying IR. 19 EMS is not a disease per se, but rather is a clustering of clinical abnormalities that, when identified collectively in a given patient, indicates that the likelihood of developing laminitis is greater than in individuals lacking the EMS criteria. Use of the term EMS is especially practical for distinguishing affected horses from those affected with either Cushing's (pituitary pars intermedia dysfunction [PPID]) or hypothyroidism, with which EMS is often confused. 19 The clinical importance of diagnosing EMS centers on the fact that recognized risk factors for laminitis can subsequently be avoided in the affected individual. Preventive measures aimed at reducing the risk for laminitis should be rigorously emphasized in EMS-affected horses and ponies.Recently, the American College of Veterinary Internal Medicine (ACVIM) commissioned a panel of EMS-interested specialists to develop a consensus statement that would help define the syndrome based on current knowledge. 20 During development of the consensus statement, contents of the working draft were presented and discussed at the ACVIM Annual Forum in Montreal, Canada and some of the following comments will be based on those discussions. 20 Ongoing experimental and clinical studies will help better define EMS (which is distinctly different to the human metabolic syndrome 21 ) in the next few years. D...
Intracranial surgery in veterinary medicine has been limited to dogs and cats; however, in select cases, extrapolation of surgical techniques used in humans and small animals can assist with intracranial procedures in horses.
Abbreviations: (CGIT) combined intravenous glucose-insulin test, (DM) diabetes mellitus, (EMS) equine metabolic syndrome, (HbA1c) glycosylated hemoglobin, (IR) AbstractAnalogous to the situation in human medicine, contemporary practices in horse management, which incorporate lengthy periods of physical inactivity coupled with provision of nutritional rations characterized by inappropriately high sugar and starch, have led to obesity being more commonly recognized by practitioners of equine veterinary practice. In many of these cases, obesity is associated with insulin resistance (IR) and glucose intolerance. An equine metabolic syndrome (MS) has been described that is similar to the human MS in that both IR and aspects of obesity represent cornerstones of its definition.Unlike its human counterpart, identification of the equine metabolic syndrome (EMS) portends greater risk for development of laminitis, a chronic, crippling affliction of the equine hoof. When severe, laminitis sometimes necessitates euthanasia. Unlike the human condition, the risk of developing type 2 diabetes mellitus and many other chronic conditions, for which the risk is recognized as increased in the face of MS, is less likely in horses. The equine veterinary literature has been replete with reports of scientific investigations regarding the epidemiology, pathophysiology, and treatment of EMS.
Background: The combined glucose-insulin test (CGIT) is helpful for evaluating insulin sensitivity. A continuous glucose monitoring system (CGMS) reports changes in interstitial glucose concentrations as they occur in the blood. Use of the CGMS minimizes animal contact and may be useful when performing a CGIT.Hypothesis: Results obtained using a CGMS are useful for the evaluation of glucose responses during the evaluation of insulin sensitivity in equids.Animals: Seven mature, obese ponies. Methods: Ponies were equipped with CGMS for determination of interstitial glucose concentrations. Glucose (150 mg/kg, IV) and insulin (0.1 U/kg, IV) were administered and blood glucose concentrations determined at (minutes after time zero) 1, 5, 15, 25, 35, 45, 60, 75, 90, 105, and 120 with a hand-held glucometer. Blood chemistry results were compared with simultaneously obtained results using CGMS.Results: Concordance coefficients determined for comparison of blood glucose concentrations determined by a hand-held glucometer and those determined by CGMS after the zero time point were 0. 623, 0.764, 0.834, 0.854, and 0.818 (for delays of 0, 5, 10, 15, and 20 minutes, respectively).Conclusions and Clinical Importance: Interstitial glucose concentrations obtained by the CGMS compared favorably to blood glucose concentrations. CGMS may be useful for assessment of glucose dynamics in the CGIT.
A n 11-year-old Lipizzaner mare was referred for lethargy, abdominal distention, coughing, and weakness of 1 month's duration. The mare had been regularly dewormed and vaccinated against tetanus, influenza, and Eastern and Western equine encephalitis. Serum agar gel immunodiffusion assay for equine infectious anemia was negative. The mare was weak, lethargic, and mildly dehydrated. Abdominal distention was prominent (Fig 1), and borborygmi were absent. Mucous membranes were pale with a capillary refill time of 3.5 seconds. Heart (86 beats/min) and respiratory (40 breaths/min) rates were increased, and rectal temperature was 99.8uF. Body weight was 605 kg, but the mare was judged to be thin. Ventral abdominal subcutaneous edema was evident. Per rectum abdominal palpation identified a nongravid uterus. Moderate anemia (packed cell volume, 21%), mild lymphopenia, and hyperfibrinogenemia (0.5 g/dL; reference range, 0.1-0.4 g/dL) were present on the CBC. Serum biochemical analysis identified hypoglycemia (glucose, 47 mg/dL; reference range, 72-114 mg/dL), azotemia (BUN, 89 mg/dL; reference range, 8-27 mg/ dL; creatinine 5 8.8 mg/dL, reference range, 0.6-1.8 mg/dL), hyponatremia (sodium, 121 mmol/L; reference range, 132-144 mmol/L), hypochloremia (chloride, 86 mmol/L; reference range, 94-102 mmol/L), hyperka-lemia (potassium, 6.3 mmol/L; reference range, 2.7-4.9 mmol/L), hypoproteinemia (protein, 4.8 g/dL; reference range, 4.9-6.9 g/dL), hypoalbuminemia (albumin, 2.1 g/dL; reference range, 2.5-4.2 g/dL), hypocalcemia (calcium, 9.9 mg/dL; reference range, 10.7-13.4 mg/dL), hyperphosphatemia (inorganic phosphate, 13.9 mg/dL; reference range, 1.9-5.4 mg/dL), hypertriglyceridemia (triglyceride, 2,720 mg/dL; reference range, 4-44 mg/ dL), unconjugated hyperbilirubinemia (3.7 mg/dL; reference range, 0.1-1.9 mg/dL), and increased serum enzyme activities (CK, 3,147 U/L; reference range, 90-565 U/L; aspartate aminotransferase (AST), 2,268 U/L; reference range, 205-555 U/L; lactate dehydrogenase (LDH), 32,582 U/L; reference range, 520-1,480 U/L; gamma glutamyl transferase (GGT), 59 U/L; reference range, 12-45 U/L). Urinalysis indicated dilute urine (urine specific gravity [USG], 1.016) and hyaline casts (15 to 20 casts per low power field) were observed. The bladder was normal on endoscopic examination. Abdominal ultrasonography identified a large volume of anechoic abdominal fluid and revealed irregular cauliflower-like masses adherent to the abdominal wall at many locations, evidently fused to the peritoneum and characterized by mixed echogenicity (Fig 2). Other smaller masses were identified on the surface of the mesentery and adjacent to the dorsal aspect of the spleen. Abnormalities were not seen in the liver, kidneys, and intestines. Mild to moderate anechoic bilateral pleural effusion was observed. Abdominocentesis yielded a large volume of serosan-guineous peritoneal fluid (PF) characterized by a normal nucleated cell count (659 nucleated cells/mL), moderately increased protein concentration (3.2 g/dL), and a hematocrit...
CASE DESCRIPTION-13 equids (10 horses, 2 donkeys, and 1 pony) were examined for signs of colic (n = 7), weight loss (6), anorexia (3), and diarrhea (2). Ten equids were evaluated in the fall (September to November). Seven equids had a history of persimmon ingestion. CLINICAL FINDINGS-A diagnosis of phytobezoar caused by persimmon ingestion was made for all equids. Eight equids had gastric persimmon phytobezoars; 5 had enteric persimmon phytobezoars. Gastroscopy or gastroduodenoscopy revealed evidence of persimmon ingestion in 8 of 10 equids in which these procedures were performed. TREATMENT AND OUTCOME-2 of 13 equids were euthanatized prior to treatment. Supportive care was instituted in 11 of 13 equids, including IV administration of fluids (n = 8) and treatment with antimicrobials (5), NSAIDs (5), and gastric acid suppressants (4). Persimmon phytobezoar-specific treatments included dietary modification to a pelleted feed (n = 8); oral or nasogastric administration of cola or diet cola (4), cellulase (2), or mineral oil (2); surgery (4); and intrapersimmon phytobezoar injections with acetylcysteine (1). Medical treatment in 5 of 7 equids resulted in resolution of gastric persimmon phytobezoars. Seven of 8 equids with gastric persimmon phytobezoars and 1 of 5 equids with enteric persimmon phytobezoars survived > 1 year after hospital discharge. CLINICAL RELEVANCE-Historical knowledge of persimmon ingestion in equids with gastrointestinal disease warrants gastroduodenoscopy for evaluation of the presence of persimmon phytobezoars. In equids with gastric persimmon phytobezoars, medical management (including administration of cola or diet cola and dietary modification to a pelleted feed) may allow for persimmon phytobezoar dissolution.
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