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Internal Medicine/Reproduction Proceedings 2015

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Internal Medicine/Reproduction Proceedings 2015 Internal Medicine and Reproduction 2015 Program Proceedings Seventh Annual Symposium From Our Practice to Yours September 23rd - September 26th, 2015 Northeast Association of Equine Practitioners 1 NEAEP Mission Statement The mission of the NEAEP is to improve the health and welfare of horses byproviding state- of-the-art professional education and supporting the economic security of the equine industry by complementing established local associations and giving equine veterinarians, farriers, technicians, veterinary students and horse owners a unified voice at the state and regional levels. 2 2015 Internal Medicine/Reproduction Table of Contents New Strategies For Managing Neonatal Maladjustment Syndrome. Peter R. Morresey..................................4 Update on Anaplasmosis – Made No Better by a Name Change. Peter R. Morresey .....................................10 Head Shakers – Is There Anything New Under The Sun? Peter R. Morresey .................................................14 Managing Strangles Outbreaks Ashley G. Boyle..............................................................................................21 Strangles- Unusual Cases and Effective Treatments Ashley G. Boyle .............................................................25 Diagnosis and Management of the Sick Foal in the Field Ashley G. Boyle ......................................................28 Treating Colitis In The Field. Rose D. Nolen-Walston ......................................................................................30 Clenbuterol – The Good, The Bad, And The Ugly Rose D. Nolen-Walston ......................................................37 Equine Blood Transfusion - What You Need To Know To Get The Job Done. Rose D. Nolen-Walston ......................................................................................................................................41 Guttural Pouch Disease- More Than Strangles Rachel Gardner .....................................................................46 New Thinking on Gastric Ulcer Diagnosis and Treatment Rachel Gardner ......................................................50 Evaluation and Management of the Recumbent Horse Rachel Gardner .........................................................54 Nonexertional Rhabdomyolysis Stephanie J. Valberg ....................................................................................56 Exertional Rhabdomyolysis - Causes of Poor Performance Stephanie J. Valberg .........................................65 Equine Genetic Diseases - Genetic Testing: What Is Available And When To Use It Stephanie J. Valberg ..........................................................................................................................................71 The Pleurals and the Peritoneals: Body Cavity Cytology Tracy Stokol ............................................................78 A Case-Based Approach to Equine Blood Tracy Stokol ..................................................................................83 The ABCs of Acid-Base Analysis or the View from the Eye of a Clinical Pathologist Tracy Stokol ........................................................................................................................................................96 Non-traditional therapies for endometritis: science or voodoo? Charles F. Scoggin ........................................102 The impact of aging on fertility, pregnancy, and offspring vigor in broodmares Charles F. Scoggin ................108 The benefit of routine monitoring and supplementation of progesterone in early pregnancy Charles F. Scoggin .............................................................................................................................................114 Management of mares for breeding with frozen semen: pre- and post-insemination considerations for maximum fertility Kristina Lu .............................................................................................................................................118 How to successfully integrate assisted reproductive techniques in your busy practice Kristina Lu...........................................................................................................................................................124 Diagnostic methods and interpretation for endometritis Kristina Lu .................................................................129 3 New Strategies For Managing Neonatal Maladjustment Syndrome. Peter R. Morresey BVSc MACVSc DipACT DipACVIM (LA) Rood and Riddle Equine Hospital, PO Box 12070, Lexington, KY 40580 Introduction Neonatal Maladjustment Syndrome, Hypoxic-Ischemic Encephalopathy, or Perinatal Asphyxia Syndrome: foals poorly adapted to extrauterine life have been categorized in many ways. Clinical manifestation can be subtle or profound. This talk will summarize current literature explaining what is happening in these foals, provide insights into the things we can change and those we can’t, and walk through the author’s approach to these cases. Pathophysiology of Neonatal Maladjustment Syndrome Cerebral ischemia may result from systemic hypoxemia depressing myocardial performance. Reduced cerebral blood flow results in decreased delivery of oxygen and energy substrates to the brain resulting in a combined hypoxic-ischemic insult. Anaerobic metabolism depletes the brain’s stores of glucose and high energy phosphates (ATP and phosphocreatine) with resulting accumu- lation of lactate and inorganic phosphate. (Yager, 1992) Energy failure impairs glutamate uptake resulting in extracellular accumulation leading to tonic overstimulation of postsynaptic excitotoxic amino acid receptors (excitotoxicity). Reperfusion and reoxygenation in the early post-ischemic recovery period following this insult is itself harmful. Maternal infection has been shown strongly associated with neonatal brain injury. (Willough- by, Jr., 2002) Intrauterine infection may indirectly injure the brain via the induction of sepsis and poor perfusion, or directly by the production of inflammatory mediators that devitalize neurons. (Eklind, 2001) The neonatal brain has been experimentally shown as highly susceptible to free radical-me- diated injury. (Edwards, 1997) Under normal conditions, mitochondrial function generates low concentrations of the superoxide anion and hydrogen peroxide. These are scavenged by multiple enzyme systems including superoxide dismutase, catalase, and glutathione peroxidase. Other nonenzymatic antioxidants include a-tocopherol (vitamin E) and ascorbic acid (vitamin C). During reperfusion following ischemia, oxygen free radicals react with membrane phospholipids to form oxidized lipids with pro-inflammatory actions. (Grow, 2002) Regardless of the inciting cause, neural injury results in increased release of neurotrans- mitters that in turn generates an excess of second messengers, apoptosis and increases in in- tracellular sodium and calcium. (Grow, 2002) Accumulation of sodium concurrent with failure of energy dependent cell membrane ion pumps (e.g. Na+-K+ ATPase) leads rapidly to cell swelling. Accumulation of calcium due to glutamate excess and mediated by NMDA receptors can lead to activation of calcium-dependent phospholipases, nitric oxide synthase, and proteases. Increased activation of phospholipase A2 (PLA2) in postsynaptic neurons results in increased free arachi- donic acid and PAF, enhancing glutamate-mediated neurotransmission and further potentiating NMDA receptor activity, while decreasing glutamate reuptake. Cerebral ischemia induces cyc- lo-oxygenase-2 (COX-2) expression facilitating metabolism of arachidonic acid to inflammatory lipid mediators. A self-reinforcing cycle is therefore initiated. (Arundine, 2004;Bazan, 1995) A number of equine neonatal studies have shown the presence of intracranial hemorrhage associated with neurological compromise. Compared to a control group, convulsive foals showed hemorrhage in various locations of the brain. (Palmer, 1975) Also present was necrosis of the 4 cerebral cortex, diencephalon and brain stem. Minimal hemorrhage occurred in the brains of control foals. In another study, central nervous system hemorrhage was found more frequently in premature foals when compared to those born at full term, in foals born dead compared to live births, and in foals born following assisted delivery compared to foals born without intervention. Clinical presentation of Neonatal Maladjustment Syndrome The most common neurological problems of foals include depression, seizure activity, ab- normal behavior, loss of affinity for the mare and loss of the suckle reflex. All these signs are referable to dysfunction of the brain. Expression of neurological lesions will be dependent on the stage of development which the inciting damage occurred. The result of cerebral hypoxic or ischemic insult to the neonate, NMS/HIE/PAS is arguably the most common seizure precipitating syndrome faced by the equine clinician. The diagnosis is dependent upon a compatible history and clinical examination findings while ruling out other con- ditions. (Green and Mayhew, I. G., 1990) Excitatory amino acids, calcium ions, free radicals, nitric oxide, pro-inflammatory cytokines and products of lipid peroxidation are all thought to contribute to the syndrome, with the neonatal brain having an increased susceptibility to damage by these agents compared to adults. (Anderson, 1988;Arango, 2006;Arundine, 2004) In addition to neurological manifestations respiratory compromise,
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