Week 8 Notes for ANEQ 346
Week 8 Notes for ANEQ 346 ANEQ 346
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This 13 page Class Notes was uploaded by Alia Coughlan on Friday October 14, 2016. The Class Notes belongs to ANEQ 346 at Colorado State University taught by Dr Hess in Summer 2016. Since its upload, it has received 4 views. For similar materials see Equine Disease in Equine Science at Colorado State University.
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Date Created: 10/14/16
Week 8 Notes for ANEQ 346 10/10 Quiz 3 Laminitis Lecture Laminitis Extremely Painful Common in overweight ponies & insulin resistant horses Consequence to severe disease Impaired blood supply to the foot Destroys microstructure of the hoof Detachment of dermis and epidermis *Often happens to both feet at same time *Poorly understood pathogenesis *The more areas in the foot that get separated, the more severe the laminitis is Causes of Laminitis Nutrition related: Grain overload Can happen to any horse Soluble carbohydrates in hindgut Endotoxin/exotoxin Trigger arterial shunts Often poor outcome Lush pastures Overweight and thin horses Soluble and fermentable carbohydrates in hindgut Metabolic causes triggered by nutrition: Cushings, insulin resistance, obesity Clinical Signs Prodromic period is from time of ingestion till the time when signs begin to show Clinical signs might not show up till 1220 hours after ingestion Shifting from foot to foot Increased digital pulse Increased hoof temperature – can check hindlegs for comparison Difficulty turning Lameness Inability to walk Laying down Diagnosis Clinical signs Hoof tester Xrays Rotation Prognosis is related to the degree of rotation Pulls on coffin bone and detaches the dermis and epidermis Pulls from deep digital flexor tendon Treatment Don’t force them to move Deep bedding Frog support Pain killers Antiinflammatories *Studies show that if horse has early signs of laminitis, to put them in ice water for 72 hours. Laminitis will go away 10/12 *Insulin resistance = insulin is unable to increase glucose entry into insulin sensitive cells High Insulin = induced laminitis intravenously Acute Treatment of Laminitis Immobilization of affected structures Rest NSAIDS Deep bedding Clean foot If possible, remove the shoe Relieve the pressure on the toe Bandages, pads, support of sole Relieves the pressure on the deep digital flexor tendon Prevent coffin bone from rotating If it does the laminitis will be chronic Should do daily monitoring of coronary band with radiographs every 7 days Chronic Treatment of Laminitis Restructuring of foot Trim Heel elevation Sole and axial support Improved brake over *Only restructure foot when you can pick it up without pain Laminitis Management Low NSC hay!!!!!! Laminitis Prevention Know causing factors Dietary contribution ~ at least 56% Soluble carbs~ starches, simple sugars, grass cuttings Limit amount of grazing Grazing muzzle Obesity Insulin resistance *Grasses accumulate energy in the form of fructan *Lumens accumulate energy in the form of starch Muscle Problems Lecture HYPP Hyperkalemic periodic paralysis Codominant single autosomal genetic disorder Impressive = the horse who spread this disease thru breeding Both heterozygous (H/N) and homozygous (H/H) show signs Affected gene is the sodium channel It facilitates movement of K+ into the cell, and Na+ out of the cell With HYPP: Constant back leakage of sodium into the cell with K+ outside cell higher Muscle fasciculation’s – membrane potential Clinical Signs Happens to horses who have Impressive’s genes Q horses, Appaloosas, Paints, other crosses Prolapse of membrane nictitans with or w/o facial muscle spasm and general muscle tension Between episodes, horse is normal Buckling at knees and hocks Altered vocalization Duration = 3060 min Death can occur Usually seen before 3 years old HYPP Management Limit increases in serum potassium Limit dietary potassium Promote entry of potassium into cells Main sources of K+: High fertility soil, early cute, increased moisture Grass forages vs legume forages Grain: low K+ and high insulin that drives potassium into cells Exercise also helps drive K+ Eliminate excess potassium from body via urine Exertional Rhabdomyolysis (ER) Also called “Tying Up” and “Monday Morning Disease” Very fast onset Syndrome of muscle pain and cramping associated with exercise 2 Forms of Chronic: Recurrent exertional rhabdomyolysis (RER) Intracellular calcium regulation defect: muscle necrosis during exercise TB Polysaccharide storage myopathy (PSSM) Increased storage of glycogen and abnormal polysaccharide in muscle heavy breeds, QH, WB Causes Familial predisposition Carb overloading in face of decreased exercise Metabolic pathway abnormalities Signs Hindleg stiffness Pain to palpate gluteal muscles and hamstrings Sweating, elevated HR and reluctance to move Dark colored urine Diagnosis Bloodwork CK = Creatin kinase Peaks in 6 hours AST = Aspartate aminotransferase Peaks in 24 hours, decreases in 1 week Electrolyte deficiencies Treatment IV fluids – flush kidneys DMSO NSAIDS Sedation for extreme pain Acepromazine to relieve anxiety and increase blood flow Should not travel for 2448 hours Hay diet for several days Monitor blood work for decrease in muscle enzymes *Rare for horse to only get one time *No sweet feed! Want feed high in fiber and fat PSSM Signs ER Exercise intolerance Muscle stiffness Back pain Coliclike signs *Diagnosis is thru a muscle biopsy from the hamstring muscle *May be associated with “shivers” in draft breeds 10/14 Equine Wound Management Wound Repair Begins the moment a cellular barrier is broken Has 3 main phases: Acute Inflammation Vasoconstriction and then vasodilation Blood coagulation + aggregation = fibron + cellular clot Hemostasis + scaffold for cell migration Desiccation (scab) Reparative phases Contaminants + dead tissue Needed for normal repair Fibrin provides strength Will be replaced by granulation tissue in the next phase Inflammation time excessive fibrosis and scarring Cellular Proliferation Granulation tissue and epithelialization Granulation tissue Macrophages Blood vessels Fibroblasts Red and granular appearance Begins to invade about 5 days after injury Barrier to infection “Bed” for cell migration Epithelialization Free edge Continues until wound is covered Migration ceases because of contact inhibition Do not want temperature to be too hot or cold Slows down healing process Other aspects that also slow down healing Infection, excessive granulation tissue, repeated dressing changes Matrix Synthesis and Remodeling Involves reduction of wound size and reorganization of the extracellular matrix Contraction starts in 2 week after injury Wound edges are progressively bought together Amount of wound contraction depends on site Myofibroblasts from granulation tissue Too little = poor contraction Too many = pathologic contraction At maximal strength, fully healed wounds are 1520% weaker than tissue around Primary Intention Healing Primary wound closure is preferred Heal faster, better cosmetic results Skin edges are sutured together Reduced risk of contamination Used when there is little tissue loss, wound in new Depends on vascularity and contamination Can get partial or complete wound dehiscence Should be sutured 45 days after injury Before granulation tissue forms Severely contaminated or swollen wounds Allows time to promote drainage, reduce infection and inflammation *Longer it takes to do primary closure, the higher the risk it won’t work Secondary Wound Closure Manage as an open wound Bandages and topical agents that promote initial inflammation Granulation tissue Stimulates until wound has filled in Healing often protracted Wounds that have significant tissue loss Persistent granulation Foreign bodies, wound infection, chronic inflammation Slowest phase Leaves a superficial scar *Secondary closure is delayed because wound edges close after the formation of granulation tissue Reasons for Infection Elapsed time from injury Degree of contamination Degree of tissue damage Thoroughness of wound lavage After debridement: Number of bacteria left Dead space Devitalised tissue *Ponies vs Horses Ponies have less complications when it comes to wound dehiscence and bone sequestrum Ponies have faster second intention healing Have stronger initial inflammatory response Ponies = wound contraction Horses = epithlilization Wound Management Goals: Restore function Good cosmetic appearance Minimize infection Short recovery period Depends on: Use of horse Anatomic location Severity of wound Tendon sheaths, abdominal, over joints & eyes are emergencies Degree of contamination Financial considerations Available equipment Wound first aid Prevent further injury Slow or stop blood loss Minimize contamination Cover and protect promptly Wound assessment Physical exam Control hemorrhage Severity and damage to underlying structure Local antibiotics should be given within 3 hours Wound dressings Should be moist Good environment for wound healing Enzymes from white blood cells cause autolytic debridement of wound 7296 hours – clean wound to prepare from repair phase Prevents formation of scab Reduced pH More rapid epithelialization Bacteria might proliferate Ideal wound dressing: Absorbs exudates Humidity Gaseous exchange Thermal insulation Bacterial penetration Nontoxic Easy removal *Gauze dressings are a good choice – can use wet or dry