Equine Ophthalmology Notes PDF

Lecture 1 + 2 - Equine ophthalmology Learning outcomes be able to diagnose and manage ulcerative keratitis (corneal ulcer) in the horse Be able to diagnose and manage uveitis in the horse Common equine ocular diseases ocular/periocular trauma Keratitis (ulcerative, non-ulcerative) - inflam...

Lecture 1 + 2 - Equine ophthalmology Learning outcomes be able to diagnose and manage ulcerative keratitis (corneal ulcer) in the horse Be able to diagnose and manage uveitis in the horse Common equine ocular diseases ocular/periocular trauma Keratitis (ulcerative, non-ulcerative) - inflammation of the cornea Uveitis (primary, secondary, chronic/recurrent) - inflammation of the uveal tract Ocular/periocular neoplasia Corneal stromal abscessation Cataracts Glaucoma — intraocular increase in pressure Equine ophthalmic examination Sedation - in order to be able to open the eye with less resistance - a2 agonist - Opioid agonist or agonist/antagonist e.g. butorphanol Diagnostic nerve blocks - auriculopalpebral or palpebral (motor) - Frontal (sensory) diagnostic mydriasis - mydriasis = dilated pupil - to be able to look in caudal parts of eye i.e fundus - tropicamide (hours) - atropine for therapeutic mydiasis NOT diagnostic (sensitive — will dilate for days - weeks) transillumination and retro illumination - trans: bright light directly into eye, reflects back from opacity in lens - retro: bright light, dark surrounding, shine light at angle, sees light reflected from back of eye direct or indirect ophthalmoscopy (to look at fundus) normal tapetal Fundus > /queen - large optic disc unique > - non- to horse. tapetal Fundus  Examination for FBs Fluorescein staining Culture and/or cytology of corneal swabs or scraping (+/- tropical local analgesia) schirmer tear test (assess lacrimation) Tonometry (measure intraocular pressure) Slit lamp biomicroscopy Ultrasonography - concerned about pathology in deeper parts of eye (fundus) and you can’t see all the way through - transpalpebrally (from on top of eyelid) Ulcerative keratitis = corneal ulcer associated with inflammation of the cornea Aetiology mechanical trauma Primary infectious (bacterial, fungal, viral) e.g. pseudomonas, herpes virus Decreased tear production (KCS, VII paresis) Irritants Corticosteroid-associated Diagnosis bleopharospasm (closed painful eye) and epiphora (excessive tearing) Focal corneal opacity +/- adjacent corneal oedema (w/ epithelium gone water from tear film gets into stroma) +/- keratomalacia Fluorescein (positive unless descmetocoele - ulcer eroded all the way through Stroma only one layer of endothelium left) +/- corneal neovascularisation +/- concurrent anterior uveitis ulcer ↓ cornea Jedema Ketaomalacia ↑ - meltinge - strom Ancillary diagnostics examination for causes of mechanical trauma e.g. FB Corneal swab/scraping for cytology and bacterial/fungal culture Fundic examination +/- schirmer tear test, slit lamp exam and/or tonometry  nations common Management ↓ more Topical antimicrobial (antibacterial +/- antifungal or antiviral) drugs ointments or solutions Direct application - Lavage system (subpalpebral or nasolacrimal) - different methods Sub-conjunctival - of application Topical atropine mydriasis and cycloplegia (getting rid of spasm of ciliary body) for analgesia Prevention of synechiae (adhesions between bits of eye) Similar routes of administration to antimicrobials Solution or ointment System NSAIDs analgesia and anti-inflammatory actions Flunixin meglumine (best), phenylbutazone, ketoprofen PO or IV (not topical as can be irritant) Face mask with solid eye cup protect eye from self trauma avoid photophobia (atropine) Topical anti-collagenase therapy to treat or prevent keratomalacia plasma/serum EDTA/heparin - MOST COMMON tetracyclines Acetylcysteine Hyaluronic acid Topical application or via lavage system Surgical intervention tarsorrhaphy —> suture eyelids together Nictitans/third eyelid flap —> third eyelid pulled over ulcer Conjunctival flap —> resected conjunctiva put over ulcer and sutured to cornea (specialist) Enucleation Additional therapies systemic antimicrobial drugs ocular lubricants Therapeutic contact lens Indolent superficial ulcers non healing Debridement Grid keratectomy Chemical cauterisation/irritation therapeutic contact lens Surgery Prognosis healing of corneal ulceration - if superficial —> re-epithelialisation - if deep —> neovascularisation,granulation tissue, fibrosis (will have scar) corneal scar formation or pigmentation - permanent visual deficits - melanocytes come with neovascularisation and stay after prognosis poor for fungal infections, ulcers with significant keratomalacia and descmetocoeles Concurrent uveitis may cause permanent visual deficits or become recurrent Duration of therapy — days to weeks + $$$$ Enucleation - consequences for racehorses Equine Uveitis = inflammation of the uveal tract (iris, ciliary body, choroid) very common in horses May be acute and completely resolve or become chronic or recurrent Aetiology trauma Immune-mediated — e.g. rhodococcus equi, strangles Secondary to corneal disease Primary infectious (bacteria, fungal, viral, parasitic) — leptospira, onchoceriasis Diagnosis peri ocular swelling, blepharospasm and epiphora (same as ulcer) Scleral and conjunctival injection/hyperaemia +/- chemosis (bulging oedematous conjunctiva) Miosis (constricted pupil) Aqueous flare (protein) , hypopyon (pus/ fibrin) or hyphaema (blood) — abnormality in anterior chamber - with aqueous flare can see beam of light going through anterior chamber - these signs are pathognomonic for anterior uveitis +/- diffuse corneal oedema (fluorescein negative unless concurrent corneal ulceration) and corneal neovascularisation - diffuse corneal oedema give eye blue appearance Ancillary diagnostics examination of signs of external trauma Fundic examination Investigation of systemic disease or ocular infections +/- slit lamp examination +/- tonometry +/- anterior chamber paracentesis (culture, cytology) Posterior uveitis on fundic exam can see small scars on choroid Indicates previous posterior uveitis & > Management of acute uveitis Anti-inflammatory therapy - corticosteroids topical and/or systemic CAN use these DO NOT use if corneal ulceration present in concurrently horses Anti-inflammatory therapy- NSAIDs systemic and/or topical Topical atropine mydriasis and cycloplegia for analgesia Prevention of synechiae Face masks with solid cup protect eye from self trauma avoid photophobia +/- antimicrobial/antifungal drugs (topical or systemic) +/- cyclosporine (topical) +/- treatment of primary ocular or systemic disease Management of Chronic uveitis Corticosteroids and/or NSAIDs Cyclosporine (topical or intra-vitreal implants Chemical ablation of ciliary body Surgical vitrectomy Enucleation Sequelae to acute uveitis chronic or recurrent uveitis Glaucoma, synechiae, cataracts, choroidal and/or retinal degeneration, chronic corneal disease Chronic ocular pain Blindness - > most common Phthisis bulbi — end stage eye, small shrunken and a-visual - Prognosis poor if acute uveitis is not adequately controlled Poor in cases of chronic or recurrent uveitis Enucleation may be necessary in cases accompanied by chronic pain Prevention vaccination for leptospira interrogans serovar pomona in USA - 2 doses 3-4 wks apart then annual booster - lepto EQ innovator parasite control for onchocerca Lecture 3+4 - Clinical parasitology Major parasites in equine large and small stongyles Roundworms (ascarids) Tapeworms Pinworms > less significant Bots Strongyles strongyle adults occur in the large intestine Treatment: ivermectin, moxidectin, pyrantel large stronglyes highly pathogenic (migrate through body) Uncommon the most important nematodes of domestic equines throughout the world Teeth and cutting plates are used to chew on migrate through the body and end up in the wall of the arteries that feed the gut PPP 6-10 months Small strongyles (cyathostomines) pathogenic (do not migrate - stay in gut) Very common (drench resistance) currently the most important parasitic disease of horses Affect all grazing horses Infections are acquired from pasture only (not stalls or dry lots) Eggs hatch at temperatures 7-29 degrees (>30 larva die, resistant to freezing) life cycle includes cystic stafe in large intestine mucosa where parasites imbed themselves something triggers them and they emerge from mucosa (L4) —> severe inflammation  1-1.5 cm red worms PPP difficult in horses as can encyst in mucosa for up to 2.5 years can stay hea ↓ up to 2 5 years. larvae causes a protein losing disease that leads to muscle wasting and oedema Disease occurs on emergence of larvae Are resistant to benzimidazole drugs Round worm - parascaris equorum mostly seen in foals carried by circulatory system to liver and lungs —> break through blood vessels and migrate up trachea —> coughed up and swallowed again Mature in small intestine, PPP 10-12 weeks Longevity ~2 years eggs are very resilient with sticky walls Heavy burdens persist for 9 months and can block the intestine —> ill thift Liver and lung migration may lead to clinical signs Resistance to ivermectin, Oxfendazole, benzimidazole considered to have good activity Pinworm - Oxyuris equii male 1cm long, females 10cm direct lifecycle, but lay eggs on perineum Cause horse to rub behinds especially in stabledhorses Diagnosis with sticky tape Distribution of egg counts across individual horses parasites are not equally distributed in a population Very few horses are producing a lot for the eggs (supershedders) — often no clinical signs - wont to get rid of these horses or manage separately most horses are below the threshold 80:20 problem — roughly 80% of consequences come from 20% of causes saves money and prevents drug resistance objective: limit the intake of infective larvae so that there is not effect on health of host worm pin Drenching drenches should be used as infrequently as possible in order to gain maximum effect instead of using a threshold split the population FEC into 80:20 Drenching for cythosthomines No drench will remove all the stages The inhibited larvae (in mucosa) will remain intact, re-supplying new larvae into the lumen FWEC = 0 does not mean there are no cyathostomines the lumenal form that is being removed is not what is causing disease Egg reappearance period (ERP) time after anthelminthic treatment that it takes for inhibited cyathostomine larvae to be recruited from mucosa to lumen and begin “significant” egg shedding - significant means >10% of the average initial pre-treatment FEC evaluates existence of early conditions for emergence of resistance (NOT resistance) used for cyathostomines A shortened ERP is considered a reflection of emerging resistance In practice knowing the ERP in the field helps you to rotate available anthelminthics to prolong their activity and slow development of resistance Do repeat FEC to determine Faecal egg count reduction test N=1 is never good, avoid it, don’t use it as evidence of resistance N = 6+ with equal FWEC, age, nutritional status are used to argue about resistance Aim to achieve 90% reduction in egg output, and maintain low FWEC Targeted/selective drenching - drench only some and no need to move Testing recommendations 1. Determine egg counts in faecal samples collected from 6+ horses prior to deworming 2. Perform quantitive faecal exam and calculate efficacy (FECRT) by formula (pre-count - post count)/ pre-count X 100 3. Collect faecal samples from same horses 2 weeks intervals after deworming Lecture 5: Equine gastrointestinal anatomy Gross Exterior features The stomach relatively small, J shaped, situated in the dorsal abdomen on the left. The cardiac sphincter is “tight” and the oesophagus empties into the region of the stomach lined by squamous mucosa. The latter is separated from the glandular mucosal area below by the margo plicatus. The stomach empties via the pylorus into the small intestine. Dorsally bulging blind sac Small intestine The small intestine is 20+ metres long in adult large breed horses, and is divided into duodenum, jejunum and ileum. The descending duodenum runs caudally on the right and then crosses to the left caudal to the root of the mesentery. The ascending duodenum runs cranially on the left dorsally to become the jejunum. The duodenum is fixed in position by short mesoduodenum The jejunum is located predominately on the left, dorsally from the caudal surface of the stomach to the inlet to the pelvic canal. the jejunum is less fixed due to long mesojejunum At the end of the jejunum there is a anti-mesenteric fold on the opposite side to the mesojejunum he beginning of this marks the start of the ileum The ileum passes from left to right to join the medial surface of the caecal base at the ileocaecal orifice/ valve. Caecum The caecum is a large comma-shaped blind-ended sac located on the right of the abdomen. It is >1 metre in length in adult large breed horses consists of a base, body and apex. The base is located in the right paralumbar fossa and extends craniodorsally. The caecal body curves ventrally and towards the midline, so that the apex lies on the ventral abdominal midline pointing cranially. highly sacculated (haustrae) with four taenial bands. The caecal base empties into the ascending colon (right ventral colon) via the caecocolic orifice. Colon Ascending colon The ascending (large) colon is complex and 3-4 metres in length in adult large breed horses. consists of 4 segments, separated by three flexures. The right ventral colon runs cranially on the right from its origin at the caecal base. In the cranioventral abdomen it crosses from right to left at the sternal flexure (a.k.a. the ventral diaphragmatic flexure) and becomes the left ventral colon. This runs caudally in the left ventral abdomen, and on reaching the inlet to the pelvic canal it narrows significantly and turns 180 degrees at the pelvic flexure and beocmes the left dorsal colon. The left dorsal colon is attached to the left ventral colon by mesocolon. It runs cranially on the left above the left ventral colon and on reaching the diaphragm crosses from left to right at the diaphragmatic flexure (a.k.a. the dorsal diaphragmatic flexure) to become the right dorsal colon. This runs caudally on the right above the right ventral colon, narrows and crosses from right to left cranial to the root of the mesentery to become the transverse colon. The right and left ventral colons are highly sacculated (haustrae) and have four taenial bands similar to the caecum.  The left dorsal colon is initially non-sacculated with only one taenial band, but prior to the diaphragmatic flexure it becomes sacculated (haustrae) and has three taenial bands. The right dorsal colon is sacculated (haustrae) with three taenial bands. Except at its origin and termination the ascending colon is free in the abdomen, which predisposes to large colon volvulus and displacement. Descending colon The descending (small) colon is 3+ metres in length in adult large breed horses. It has two taenial bands (one mesenteric and one anti-mesenteric) and is highly sacculated (haustrae) The descending colon is located predominately in the left caudodorsal abdomen. It ends at the inlet to the pelvic canal and continues as the rectum to the anus. Problems with horse intestines many segments can move around in abdominal cavity When operating you must be able to recognise the intestinal elements regardless of position - features into haustrae, taeniae, fixed position, diameter dorsal diagragmatic flexure & - Ventral diaphragmatic ract - or ↑ pelviseuve % Caudal large coording colon Gross interior features Stomach the lining of the stomach has 2 discrete components at pyloric end — glandular gastric mucosa at cardiac/blind end — non-glandular mucosa, consists of stratified squamous epithelium Junction between mucosa is abrupt - Norandular mucosa glandular - mucosa bot flies larvae like to attach to wall of stomach and build up here The thick cardiac sphincter means any build up of pressure in the stomach makes it difficult for the horse to relieve that pressure due to limitations vomiting or erupting gas Commonly see the stomach rupture due to this Important to worm and insecticide horses Duodenum within the walls of the cranial part of the duodenum there are 2 raised mounds (major and minor duodenum papillae) —> where the pancreatic duct and accessory pancreatic duct open the common bile duct also open here of the major papillae (hepatopancreatic ampulla) Caecum ileum opens into base of caecum on a slight raised mound (ilieal papilla) adjacent to this is where the colon exits the caecum (caecocolic orifice)  Lecture 6: Equine Gastrointestinal Examination this ! know Visceral projections on RIGHT abdominal wall R. paralumbar fossa (last rib and tuber coxae) > - Base of caecum & · Hear llecacel valve here 7 know these Visceral projections on LEFT abdominal wall L. paralumbar fossa · mix of jejuum + descending colon - know these  Ventual view Dorsal view Cr Car Nasogastric intubation Indications diagnostic - detect the presence of gastric reflux or gas Therapeutic - removal of gastric reflux or gas - administration of medications, fluids or nutrition Anatomy external naris Ventral nasal meatus (only direct communication) Nasopharynx Oropharynx Oesophagus (must swallow) Gastric cardia Stomach Refluxing procedure to create siphon Fill tube with liquid then place tube below pool you are trying to get liquid out of (stomach) - want to know exact amount of liquid you put in so you can measure amount coming out - can fill tube with syringe, pump or funnel Net reflux (amount put in - amount pulled out) - anything greater than 1L is significant Position of tube (oesophagus vs trachea) see tube —> see tube move down left jugular furrow Palpate tube Shake trachea —> if tube in trachea you will here it moving aroun Listen to tube —> in oesophagus: gurgling, in trachea: breath sounds Blow into tube —> in trachea: no resistance, in oesophagus: resistance (collapsed tube) suck on tube —> in trachea: suck air, in oesophagus: resistance, can’t suck Ease of passing tube —> resistance in oesophagus, no resistance in trachea Coughing?? —> most of the time will cough in trachea but not always Complications epistaxis —> most common, going in or coming out, bucket under nose and towel over nose Aspiration pneumonia —> when tube in wrong place and something placed in tube Rhinitis, pharyngitis, laryngitis —> commonly in multiple NG tubes placed or indwelling NG tube Oesophageal or gastric perforation Breakage of nasogastric tube —> put in warm water before use, in good order Rectal palpation Indications colic or other gastrointestinal disease Reproductive and pregnancy examinations Investigation of weight loss should only be performed when safe for operator and horse Digital rectal in foals, miniature horses GI disease that can be felt on rectal palpation distension (ingesta, gas, fluid) of GIT Abnormal position of GIT Taut taenial bands (indications that intestines are distended) Faecal consistency and volume of ingesta Assessment of non-GI viscera Anatomy you can palpate rectal mucosa bony pelvis cervix, uterus, ovaries (filly or mare) Accessory sex glands (colt or stallion) Bladder and urethra Internal inguinal rings (colt, stallion or gelding) Terminal aorta, internal and external iliac arteries Left, right and ventral abdominal walls Small colon (usually containing faecal balls) Pelvic flexure Caudal border of spleen Caudal pole of life kidney nephrosplenic space cranial mesenteric artery root Caecal base Ventral caecal band (taenia) ** should NOT feel stomach (too far cranial) or intestines (if feel means distended) Complications rectal tears —> mucosal (create blood but no issues), full thickness grade 4 (life threatening) Abdominocentesis Indications colic, peritonitis, colitis Weight loss FUO (fever of unknown origin) Technique site —> most ventral point of abdomen, standing, right hand side slightly off midline or midline gross examination of colour and consistency —> assess in field, straw transparent colour Difficult to assess volume Laboratory assessment - TP, TNC (total nucleated cell count), Cytologic examination Needle (hypodermic or spinal) vs teat cannula (blunt) allow fluid to drip out (dont pull out fluid) Complications enterocentesis —> needle into intestine (remove needle immediately) Haemorperitoneum or splenic haematoma Laceration of abdominal viscus Peritonitis Subcutaneous swellings/infections Contamination of peritoneal fluid sample with blood or GI content Other diagnostics PCV/TPP Haematology and biochemistry Blood lactate concentration (measure of cardiovascular status) Faecal analysis Imaging — U/S, radiography (not useful unless mineralised) Endoscopy Intestinal absorption tests Rectal mucosal biopsy Lecture 7: Equine endocrine disease Pituitary Pars intermedia Dysfunction (equine Cushing disease) Pituitary dependent hyperadrenocortism (purely defined to pituitary gland) Signalment Most common in older equines - mean age ~20 - rare in horses pituitary releases ACTH the HP axis is critical for evoking biological responses to stressors Activation of HPA and sympathetic NS —> adrenal secretion of corticosteroids and cateocholamines dysregulation of the HPA axis include: - PPID in horses - sepsis/septic shock - central diabetes insipidus - syndrome of inappropriate antidiuretic hormone Pituitary pars intermedia dysfunction The ACTH from the pars intermedia is not released into blood stream - Pars distalis produces ACTH —> stimulates glucocorticoid in adrenal gland a single cell type here: melanotrope Produces POMC (melanin production) Directly innervated by dopaminergic neuron’s of the hypothalamus POMC —> ACTH —> a-MSH, CLIP, b endorphins (hair colour, hair growth) dopamine released by the hypothalamus has inhibitory function on pars intermedia melanotropes - regulates ACTH from the pars intermedia - stimulated by TRH Pathophysiology - PPID Loss of dopaminergic innervation of the pars intermedia —> abnormal increase in ACTH production - loss of inhibition - excess production of ACTH and related hormones (e.g. a-MSH - hair related)  ACTH from pars intermedia usually dont come out of gland and are converted to other hormones In PPID ACTH can spill out into blood steam due to increased production —> adrenal gland produces more cortisol the reason for the lack of dopamine innervation is unknown —- could be primary hypothalamic disease (not produced) or primary pituitary disease (cant uptake) horses with PPID have hyperplasia of the pars intermedia - 1 single large adenoma - multiple small adenomas oxidative stress thought to contribute to neuronal damage and cell death in both hypothalamus and pars intermedia (both hypo and pars I affected) - reduced dopamine concentration in pars intermedia - reeduced dopamine nerve terminals in pars intermedia - 50% reduction in dopaminergic cell bodies in periventricular nucleus of hypothalamus Clinical signs Polyuria/polydipsia 30% of PPID horses exhibit PU/PD Partial central diabetes insipidus (pituitary adenoma expanding into neurohypophysis – reduce ADH?) Increase thirst due to hypercortisolemia Osmotic diuresis from glucosuria (from hyperglycemia) Hyperglycemia - increased cortisol —> increased gluconeogenesis - decrease utilisation of glucose by cells Hirsutism long curly coat, fails to shed in sumemr Early in disease: lower jaw, base of neck, palmar/plantar of lower limbs Overtime: generalised, lighter coat colour Hyperhidrosis sweating thermoregulatory response to long hair coat Direct elevation of POMOs Muscle atrophy and pot belly excess glucocorticoid increase protein catabolism and muscle weakness Abnormal fat distribution cresty neck, tail head, sheath/mammary glands, supraorbial space Insulin resistance and chronic laminitis Delayed wound healing, increased secondary infection sub solar abscesses Sinusitis Silent bronchopneumonia Docile/lethargy increased plasma and CSF concentrations of b-endorphines Hyperlipaemia cortisone altering how the body metabolises fat Rare Diagnosis signalment and clinical signs in classical cases “gold standard” - post mortem examination of pituitary gland - gross enlargement of pituitary - histopathology - +/- adrenal cortical hyperplasia Dexamethoasone suppression test Obtain baseline cortisol sample Administer 40mg/kg dexamethasone IM Obtain serum cortisol value 17-19hours after dex administration Normal: serum cortisol @ 19hrs 27.6nmol/L (1mg/dL) In normal horses, ACTH release from pars distalis is inhibited by dexamethasone, resulting in cortisol suppression from adrenal In PPID horses, dexamethasone administered does not inhibit the excess ACTH released from pars intermedia (melanotropes appear to be insensitive to glucocorticoids) dexamethasone suppression test was considered antemortem “gold standard”, with claims that test approaches 100% sensitivity and specificity - true superiority of dexamethasone suppression test against other tests unproven Avoid dexamethasone suppression test in horses with history or ongoing laminitis Endogenous ACTH Collect resting Normal reference range depend on laboratory (improve overall health status, pharmacotherapy General care Clip body for hirsutism during hot months Routine dental care and correction of dental abnormalities Dietary management (geriatric feeds/feeds specific for geriatric horses with dental abnormalities) Regular hoof care and management of chronic laminitis Parasite control (regular FEC and use of anthelmintics as appropriate) Management of recurrent infections (esp foot abscesses and sinusitis) Pharmacotherapy all drug therapies are life long No drug therapy likely to completely halt progression of disease Need to treat for 2-3 months before assessing efficacy/ change drug dose Monitor improvement in clinical signs Repeat DST/Endogenous ACTH to qualitatively monitor improvement Pergolide mesylate (used most commonly) Dopamine agonist Tablets, liquid Decreases ACTH concs and improves clinical signs by providing dopaminergic inhibition to pars intermedia 0.001-0.002mg/kg PO SID - Increment of 0.001mg/kg to max of 0.01mg/kg if initially appear unresponsive Adverse side effects: Anorexia, depression, diarrhoea, colic Cyproheptadine Serotonin antagonist (serotonin stimulates ACTH from pars intermedia) tables Trilostane Competitive inhibitor of adrenal cortisol production improves signs of PPID except hirsutism Beneficial on adrenal hyperplasia, no effect on pituitary hormones $$$ for horses Prognosis for life is good to excellent Many cases are managed successfully for years Provides an improved QOL in geriatric equine patients Equine metabolic syndrome (EMS) Multifactorial endocrine disease First proposed in 2002 and thought to be similar to Metabolic Syndrome in human medicine - MS are a group of risk factors that predicts CVD in humans Syndrome associated with development of laminitis in overweight or obese “middle aged” horses and ponies Risk factors Humans Equine obesity obesity Glucose intolerance Glucose intolerance Insulin resistance Insulin resistance Dyslipidemia Dyslipidemia Microalbuminuria —> chronic recurrent laminitis Hypertension —> cardiovascular disease Clinical signs of EMS regional adipocity (accumulation of fat in certain areas) Generalised obesity Insulin resistance (IR) - Hyperinsulinaemia - Hyperglycaemia Dyslipidaemia Systemic inflammation Altered blood adipokine concentrations Obesity in EMS severely affected horses have 4-5/5 BCS typically described as easy keepers - difficult to loose weight by dietary restriction Cresty neck enlargement of adipose tissues within neck region Common manifestation of regional adiposity Scoring system of 0-5 >3 detected in EMS horses Pathophysiology of EMS genetic predisposition to obesity in certain breeds (pony, Morgan, paso fino, arabians, QH) Said to have a gene mutation - thrifty genes Require fewer calories to maintain body weight Laminitis and the EMS horse endocrinopathic laminitis —> PPID, insulin resistance/EMS, pregnancy Several theroies of why EMS horses predisposed to laminitis Theory 1: glucose dysregulation as risk for laminitis EMS horses maybe hyperglycaemic Hyperglycemia directly toxic to vascular endothelial cells (glucotoxic endotheliopathy) Hyperglycemia affects endothelial regulation of vasomotor tone (constrictive) Promotes prothrombotic endothelial phenotype Theory 2: hyperinsulinaemia affects vascular endothelium Insulin important vasomediator via modulation of nitric oxide (NO) and endothelin-1 (ET-1) pathways NO is a potent vasodilator while ET-1 is vasoconstrictive Hyperinsulinaemic state promotes activation of (vasoconstrictive) pathways Lamella hypoxia and endothelial dysfunction Diagnosis of EMS History & signalment (younger than PPID) Physical examination Laboratory tests for insulin resistance: - Frequently Sampled IV Glucose Tolerance Test (FSIGT) - Euglycemia hyperinsulinemic clamp technique - Plasma insulin concentration - Combined IV glucose insulin test (CGIT) Generally difficult to perform in field, requires multiple samplings and can be costly (~700AUD for CGIT) Prevention and management Dietary management weight loss (increases insulin sensitivity) Provide hay that has lower nonstructural carbohydrate (NSC) content e.g. oaten, grass Rest lush pasture grazing/access Exercise to increase insulin sensitivity Pharmacological manipulation Levothyroxine sodium – increase metabolism and weight loss Metformin hydrochloride – increase insulin sensitivity Pioglitazone – increase insulin sensitivity Lecture 8: Liver disease Liver reserve and regeneration large reserve capacity Remarkable regeneration capacity 80% Liver disease in horses PA toxicosis (most common) Cholangiohepatitis (common) Hepatic lipidosis Theiler’s disease Manifestations of disease Icterus - generally in acute disease only - failure of uptake/conjugation or excretion of bilirubin weight loss (chronic slow decline) Neurological signs (HE) Diarrhoea - portal hypertension —> increased hydrostatic pressure in intestines? Haemorrhage - failure of clotting factor synthesis (1,2,5,6,9,10) deermatologic signs - Dermatitis due to hepatic photosensitization. - Accumulation of dermal phylloerythrin —> exposed to sunlight = skin lesions - Pruritus due to dermal bile acid accumulation (rare) Inspiratory stertor & dyspnoea Ascites - Portal hypertension due to venous blockage =.↑ hydrostatic pressure (Starling’s Law) = ascitis Change in faecal colour Hepatic encephalopathy subtle —> mild behavioural alterations, inappetence, yawning, respiratory stertor Severe —> depression, head pressing, aimless wandering, blindness, hepatic coma Pathogenesis (not examined) 1. Accumulation of GIT dericed neurotoxin ammonia - Insufficient liver metabolism of ammonia = increase plasma ammonia, x BBB to CNS - Astrocytes detoxify ammonia into glutamine. Glutamine accumulation = cerebral oedema 2. Depletion of true neurotransmitter NE & dopamine increase glucagon = increase muscle catabolism and AA (aromatic & branched chain). AAA metabolised by liver, BCAA by muscles Relative increase in AAA vs BCAA. AAA efflux into CNS Some AAA compete with tyrosine = decrease synthesis of NE & dopamine Some AAA also converted into false neurotransmitters serotonin = neuronal inhibition 3. Augmented activity of inhibitory neurotransmitter GABA-benzodiazepine system GABA reduces neuronal excitability Ammonia is synergistic with benzodiazepines. Benzodiazepine binds with GABA receptors to produce neuronal inhibition Diagnosis history Clinical signs Laboratory tests Ultrasound Liver biopsy Clinical pathology ↑ GGT (hepatocellular stasis) GLDH (hepatocellular injury) ~ Total bile acids, or ↓albumin, glucose, PTT (function) => Y InTBA = liver Failure Ultrasonography size Situation Parenchyma architecture (Echogenicity, mass, abscess) can see most of the liver on right side, not as much on left (spleen here) around 7th-14th intercostal space Compare echogenicity to spleen (liver should be less echogenic - darker) U/S guided biopsy Acute toxicosis pyrrolizidine alkaloids (PA) Mycotoxins Sporodesmin PA toxicosis many plants contain toxic alkaloids Toxicity varies with type, geography and parts of plants Toxic dose of dried plants is 5% bwt Cumulative effect (mnths - yrs) Species sensitivities differ Pathophysiology Toxic alkaloids absorbed after ingestion Transported to liver via portal circulation Metabolized by microsomal enzymes of liver by-product = toxic pyrroles Pyrroles cross-links with hepatocyte DNA (dose dependent) - more it cross links the more the hepatocytes dysfunction Hepatocyte cannot divide —> forms megalocyte, cytoplasm expands without nuclear division (ANTIMITOTIC effect) Hepatocytes eventually die, replaced by connective tissue (fibrosis) —> when you see liver failure Common examples fire weeds (senecio madagascariensis) pattersons curse (echium plantagineum) Heliotrope (heliotropium amplexicaule) Darling peas (swainsona) Diagnosis history and signalment Reported presence of PA plants CBC/MBA (most of the time haematology normal, liver enzyme increases) Liver U/S Liver biopsy and histology —> definitive NO FEVER - not inflammatory or infectious Histology of PA toxicosis megalocytes Centrilobular necrosis Necrosis of portal areas Fibrosis +/- bridging fibrosis (poor prognosis) Prognosis mild live injury (good prognosis) - appetent, no weight loss, no neurological signs, no more exposure, improving liver profile Liver failure (bad prognosis) - acute onset, inappetence, signs of HE, TBA > 50umol/L, cirrhosis and fibrosis (histopath) Cholangiohepatitis ascending infection from small intestines FEVER! (Changes in haematology) +/- weight loss Depression Dermatitis Increased GGT, ALP, GLDH Diagnosis U/S (liver tends to be brighter, rounded borders, increase in sludge in bil ducts) biopsy —> C&S Hyperlipaemia miniature horse, shetland ponies, miniature donkeys due too negative energy balance Get increase in triglyceride metabolism —> TG accumulation in hepatocytes Clinical signs depression Anorexia/inappetence Neurological signs Diarrhoea Hepatic insufficiency spin down blood and have lipemic serum Biochemistry increases in TG (triglycerides) Increases in GGT, GLP, GLDH, TBA Decrease pH Azotaemia Treatment of liver disease remove inciting cause - PA toxicosis: remove from offending pasture - hepatic lipidosis: address negative energy balance - remove drugs toxic to liver antimicrobials in cholangiohepatitis (based on C&S of blood culture/ liver biopsy) control abnormal behaviour - sedation: xylazine, detomidine nutritional support - branched chain amino acids - enteral parenteral - vitamin B complex (increase appetite) Lecture 8: Urinary tract disease in horses acute and chronic renal failure Renal failure common clinical signs Urolithiasis PU/PD Cystitis/pyelonephritis Oliguria/anuria (end stage) Urinary incontinence Hematuria/pigmenturia Hematuria/pigmenturia Weight loss Bladder rupture Renal tubular acidosis Distal urinary tract disease (bladder —>) Neoplasia pollakiuria Incontinence Discomfort/colic Hematuria Pyuria Proteinura Diagnostic tests for kidney disease Hematology/Biochemistry Urinalysis Fractional excretion of electrolytes (Na, K, Cl) Urinary Protein: Urinary Creatinine ratio BUN:Creatinine ratio Cystoscopy Rectal examination Renal ultrasound (transabdominal & transrectal) Renal biopsy Cystoscopy of bladder with bladder stone damage and haemorrhage to mucosal wall from rough stone Laboratory diagnosis Haematology/biochemistry azotaemia (increase in BUN or serum creatinine) Electrolyte imbalances (low NA or Cl, high K) Urinalysis isosthenuria (1.008 - 1.012) Proteinuria, protein cast, pyuria Fractional excretion of electrolytes (NA, K, Cl) assess tubular function Normal FE = decreased renal blood flow Toxic renal nephropathy aminoglycosides (gentamiacin) Filtered by glomerulus Binds to phospholipase on brush border of proximal tubules & reabsorbed via pinocytosis = accumulation Interferes with Na+K+ATPase, lysosomal & mitochondrial function Proximal tubular necrosis NSAIDs (flunixin, phenylbutazone) non-selective inhibition of COX1 and COX2 Inhibition of prostaglandin synthesis regulated by COX 1 Vasoconstriction and increased renal vascular resistance medullary crest necrosis Pigment nephropathy (rhabdomyolysis - typing up + severe dehydration) myoglobin is toxic to kindeys Chelates NO —> vasoconstriction —> decreased RBF & O2 tension Tubular obstruction by heme protein cast myoglobin Direct toxicity via free chelatable iron compound Vitamin D/K3 toxicity vit D —> altered Ca homeostasis, calcification of soft tissues Vit K —> acute tubular necrosis Obstructive (urolithiasis, neoplasia) not very common Treatment of renal disease Increase GFR & Diuresis IVFT (80-100ml/kg/day) - NaCl if hyperkalemia - Hartmann’s Mannitol (0.25g – 1g/kg IV over 30 min) - Osmotic diuresis (.↓ Na resorption @ tubule & collecting ducts) - ↑ vasodilatory PGs &↓ renal vascular resistance =T RBF & GFR Furosemide (1-2mg/kg IV/IM BID; 0.12mg/kg loading dose —> 0.12mg/kg/hr) - Na+K+2Cl symporter inhibitor - ↓ NaCl resorption from descending tubules =↓ H2O resorption Dopamine (3-5 µg/kg/min) Renal afferent vasodilation = increase RBF & GFR No nephrotoxic drugs! Glucose, Bicarbonate & Insulin for persistent hyperkalemia Monitor azotemia, K+ (monitor for development of peripheral/pulmonary oedema) Urinary tract infection cystitis - secondary to neurogenic (EHV-1, sacral injuries, cauda equina syndrome) - bladder injury (cystic calculi, sabulous urolithiasis) pyelonephritis Treatment for UTI Treatment of primary disease Maintenance of urine flow - IVFT, encourage oral drinking via salt licks - Drainage of bladder via catheterization Antimicrobials - Penicillin (22mg/kg IM BID) - TMS (30mg/kg PO BID) anti-inflammatories - NSAIDs eg flunixin 1.1mg/kg IV (caution: renal failure) Urolithiasis kidney — nephrolithiasis Ureters — ureterolithiasis Bladder — cystic calculi, sabulous urolithiasis (sand) Urethra — urethral calculi signalment males > females Urine: increased pH, nidus, increased crystalluria, mucoprotein, CaCo3 Diet: increased mineral content Urine stasis Decreased water intake Bacterial infection Treatment Treat primary disease Manual bladder evacuation/catheterisation Repeated flushing of bladder - Sterile Hartmann’s (~5-10L daily) - DMSO Pharmacological therapy - Bethanechol - Phanoxybenzamine Lecture 9 and 10: equine colic and diarrhoea (general principles) general principles of colic Colic = set of behavioural signs suggestive of abdominal pain depression Anorexia Recumbency Getting up and down Pawing Looking at abdomen Rolling Frequent urination (males > females) History duration and severity of colic signs Previous episodes of colic Other recent diseases and medications Has owner treated horse for current colic (what drugs, when, how much) Appetite Normal diet and any dietary changes Faecal output (quality, frequency and consistency) Weight loss (chronic) Deworming regimen (when, what, who gave it) Dentistry Physical examination signs of colic Vital signs (TPR) CV status (MM and CRT, skin Turgor, pulse quality, palpate extremities) GI sounds abnormal abdominal contour Pings Faecal consistency Evidence of self trauma Sweating Signs of non-GI disease **If the horse has severe colic you may postpone history taking and PE until you have provided analgesia ** Analgesic should be fast, limited affect on other body systems (GI, DV), last for short period of time —> Xylazine (effects other body systems but only during duration of action) if possible obtain HR, CRT, and assess GI sounds before providing analgesia Ancillary diagnostics nasogastric intubation should be performed in every case of colic Perform first after PE Leave NG tube in place (or frequent decompression) if obtain significant amounts of gastric reflex DO NOT administer anything orally or via NG tube if obtain significant amounts of reflux - tells you horse has SI or gastric outflow obstruction Rectal examination (look at previous notes) Abdominocentesis (Look at previous notes) Other tests PCV/TPP, haematology, biochemistry, blood lactate conc. FEC, U/S, endoscopy Diagnostic questions definitive diagnosis (often don’t know this) Involvement of stomach, small intestine, large intestine, non-GI organs Strangulating vs non-strangulating lesions Strangulating GI lesions blood supply to segment of intestine is compromised, leading to ischaemia and subsequent necrosis Diapedesis (movement) of RBCs through serosa of a strangulated intestine results in serosanguinous peritoneal fluid (abdominocentesis) may be associated with signs of CV compromise or endotoxaemia ALL strangulating lesions are surgical Non-strangulating GI lesions blood supply to intestine is not compromised Peritoneal fluid is not serosanguinous Usually not associated with signs of CV compromise or endotoxaemia May be medical or surgical Decision for referral referral to a hospital will enable increased level of monitoring Access to advanced diagnostics Access to advanced medical and surgical treatment Enable ambulatory clinician to continue with scheduled work Findings suggestive of referral for intensive care and/or surgery severe pain Poor response to analgesia Need for repeated analgesia CV compromise Significant gastric reflux Rectal findings suggestive of a lesion that requires intensive care or surgery Abnormal peritoneal fluid Abdominal distension (with other signs) Decreased or absent GI sounds (with other signs) ** refer early ** especially if the condition is not improving or is deteriorating Greater probability to successful outcome Transport for referral appropriate analgesia Remove any partitions in horse float (likely to lie down) Do not tie horse up in float Do not take the horse’s “friend” Do not stop No people in float with horse Analgesics DOs α2-AGONISTS – xylazine, detomidine, romifidine OPIOID AGONISTS/AGONISTS-ANTAGONISTS – butorphanol, morphine, pethidine NSAIDS – flunixin, ketoprofen (longer time of onset) BUSCOPAN COMPOSITUM SOLUTION® (spasmotic colic) DON’Ts PHENYLBUTAZONE (not good visceral analgesic, long time to produce effect) ACEPROMAZINE (not an analgesic drug, causes profound, prolonged hypotension) Repeated administration of drugs that decrease GI motility in horses with decreased/ absent GI sounds Repeated administration of potent analgesics such as flunixin (masking pain) Laxatives —> used for feed impactions Paraffin oil (mineral oil) – therapeutic and diagnostic (can see in come out if GIT patent) Magnesium sulphate (epson salts) - osmotic Dioctyl sodium sulfosuccinate (DSS, Coloxyl®) Psyllium hydrophilic mucilloid Enemas (little value in adult horse, used in foals for meconium impaction) Other therapies oral or IV fluids GI rest (no food till colic resolves) Anthelmintics(if you think related to internal parasitism) Other pharmacotherapies (e.g. prokinetics) Surgery **Most horses with acute colic will respond to medical therapy alone (i.e. analgesics +/- laxatives)** General principles of diarrhoea Diarrhoea Adult = diarrhoea most commonly a result of large intestinal disease (colitis or typhlocolitis - caecum) - if issue with SI, the LI will still absorb water and faecal balls will form Foal = Diarrhoea may be the result of small intestinal disease (enteritis) - large intestine undeveloped with limited ability to absorb excess water acute vs chronic ( hypoproteinaemia —> decreased oncotic pressure) Acute diarrhoea — Diagnosis History: Duration and severity of diarrhoea signs Previous episodes of diarrhoea Other recent diseases and medications Recent stresses Appetite Normal diet and any dietary changes Evidence of colic Other horses with diarrhoea (environmental, nutritional, infectious) Weight loss Deworming regimen Physical examination Faecal consistency and frequency of diarrhoea Vital signs (TPR) Abnormal abdominal contour Pings CV status (MMs and CRT, skin turgor, pulse quality, palpate extremities) Colic/tenesmus? Urination? Dependent oedema GI sounds Diagnostics NG intubation if signs of colic Rectal examination if signs of colic Abdominocentesis Routine haematology and biochemistry Urinalysis Faecal analysis Parasite examination Bacteriologic cultures/toxin assays/PCR Examination for sand Examination for blood Examination for leukocytes Virological tests Chronic diarrhoea — diagnosis History Physical examination Rectal examination Abdominocentesis Routine haematology and biochemistry Transabdominal/transrectal ultrasonography Intestinal absorption tests Rectal mucosal biopsy Faecal analysis same as acute diarrhoea + Examination for protozoa (should have lots of motile protozoa — if none = dysbiosis) Laboratory abnormalities Haemoconcentration Dysproteinaemias (abnormalities of TPP) Leukopaenia/leukocytosis Hyperfibrinogenaemia/elevated SAA Electrolyte/acid-base abnormalities (to determine appropriate fluid therapy) Elevated blood lactate (CV status — higher = poor circulatory system) Azotaemia Coagulopathies (if developed endotoxaemia) Complications endotoxic shock Laminitis Thrombophlebitis Disseminated intravascular coagulation Acute renal failure (ischaemic nephropathy— renal disease from insufficient blood supply) chronic malabsorption (fibrosis in GIT) Scouring Principles of therapy correct dehydration correct electrolyte and acid-base abnormalities (must take bloods to determine) Plasma or other colloids NSAIDS e.g. flunixin meglumine Fluid therapy primer: type: water, isotonic crystalloid, hypotonic or hypertonic crystalloid, colloid, additive e.g. glucose, lytes Total volume: maintenance (50ml/kg/day - adult) + deficit + ongoing losses +/- diuresis volume ↓ Possible nan by route: NG tube (intermittent) or IV (CRI), never SC or IM Rate: NGT - L/intubation, IV - L/hr or L/bolus Controversial therapies antimicrobials (refine to a few aetiologies e.g. costridosis, lawsonia) Antidiarrhoeal agents — firms up faeces (e.g. bismuth subsalicylte, smectite) Probiotics/transfaunation anti-endotoxin therapies (Polymixin B, hyperimmune plasma/serum, DMSO, pentoxifylline) Antithrombotic therapies (Aspirin, heparin) Corticosteroids (more potent anti-inflammatory) Biosecurity should assume all horses with acute D+ have infectious cause until proven otherwise Physical isolation of horses with D+ from other horses Barrier nursing Decreasing environmental pathogen load i.e cleaning and disinfection Outbreak investigation routine surveillance Lecture 11, 12 - common causes of colic and diarrhoea Colic most horses with colic will respond to medical therapy (i.e analgesics +/- laxatives) Common “medical causes of colic” many medical colics are idiopathic and will resolve without a definitive diagnosis Spasmodic colic Colic due to GI spasm Changes in diet, environment, transport, “stressful” situations, parasitism, deworming Mild to moderate colic + increased GI sounds Minimal CV compromise, no net gastric reflux, normal rectal findings, normal peritoneal fluid Rx - analgesics + correct primary problem Flatulent/Gas Colic Colic due to gas accumulation in GIT Primary (something produces gas) or secondary (GI obstruction) Moderate to severe colic + variable GI sounds Distended abdomen + pings +/- flatulence (good - helps with diagnosis and gas able to get out) May develop CV compromise (intestines can get large and compress major vessels), +/- gastric reflux of gas, gas distended GI per rectum, normal peritoneal fluid (not a strangulating lesion) Rx - analgesics, gastric decompression, +/- caecal trocharization (base), +/- surgery Large Intestinal Feed Impaction most common sites: Pelvic flexure and large colon, caecum, small colon Poor dentition, fibrous diets, parasitism, dehydration, decreased access to water, decreased exercise, foreign bodies Mild to moderate pain, decreased GI sounds, minimal CV compromise, no gastric reflux, +/- palpate impaction per rectum, normal peritoneal fluid Rx - analgesics, laxatives, rehydration, GI rest, +/- surgery for caecal and small colon impactions Meconium impaction in foals Gastric Dilation/Impaction May be primary due to dietary indiscretion or secondary to ileus or SI obstruction May rupture stomach resulting in death Mild to severe colic with variable GI sounds +/- spontaneous gastric reflux (food out nostrils - passNG tube immediately), normal rectal findings, normal peritoneal fluid (unless ruptured) Rx - analgesics, gastric decompression, gastric lavage for impactions Gastroduodenal Ulceration Associated with “stress”, other diseases, NSAID drug Rx, high concentrate diets, infrequent feeding, restricted access to pasture, exercise Mild to moderate colic, with variable GI sounds Many have no clinical signs No gastric reflux, normal rectal findings, normal peritoneal fluid, +/- colic after eating, gastroscopy Rx - removal of stress, dietary change, anti- secretory drugs (omeprazole, ranitidine), analgesics (don’t want to give NSAIDs if think this is the cause) most commonly seen in squamous mucosa and junction (margo plicatus) Complications in adults uncommon except colic, more common in foals Colitis, Typhlocolitis, Enteritis Peritonitis inflammation of the peritoneal cavity Primary (e.g. Actinobacillus through haematogenous spread) secondary to GI perforation, abscessation, penetrating wounds, uterine rupture, infection of non-GI viscera Mild to moderate colic, variable GI sounds, +/- CV compromise, fever, gastric reflux if have ileus, abnormal rectal findings, abnormal peritoneal fluid, abnormal haematology, ultrasonography Rx - analgesics, Rx primary disease, antimicrobial Rx, fluid Rx, anti-endotoxin Rx, peritoneal lavage, +/- surgery Sand Colic Sand is ingested and accumulates in the large colon Can either irritates mucosa casues inflammation or cause physical obstruction/displacement Mild to severe pain, +/- diarrhoea/endotoxaemia, CV compromise, no gastric reflux, usually not palpable per rectum, abnormal peritoneal fluid Diagnosis - history (living environemnt), auscultation of ventral abdomen, faecal examination, radiography (mineralised) Rx - analgesics, fluid support, laxatives, psyllium hydrophilic mucilloid, husbandry changes (not feeding on ground), +/- surgery Sand test —> put sand in rectal sleeve, fill rest on hand with water, twist the top and leave — sand will fall into fingers before poo does. Accumulates in right dorsal colon Gastrointestinal Rupture Stomach most likely to rupture secondary to extreme dilation with gas, fluid or ingesta (usually ruptures along the greater curvature) Often decreased pain immediately post-rupture followed by marked depression, severe CV compromise and ileus due to septic peritonitis Abnormal peritoneal fluid (GI contents), +/- “gritty” peritoneal surfaces and/or free gas per rectum, +/- ultrasonography Rx-euthanasia only option Non-GI Causes of “Colic” Hepatic disease Intra-abdominal haemorrhage Urogenital disease Pleuropneumonia Laminitis Oesophageal obstruction Parturition Common surgical causes of colic Small Intestinal Strangulation Volvulus (twisting on itself) Strangulating lipomas (most common in older, usually fat, horses and ponies) Mesenteric rents (hole) Epiploic foramen entrapment Hernias +/- Intussusception (most common in foals) +/-Adhesions  results acute severe colic, +/- decreased GI sounds, large volume gastric reflux, CV compromise, SI distension per rectum, serosanguinous peritoneal fluid Rx - surgery and intensive medical therapy Prognosis - poor to guarded depending on length of SI that is strangulated - frequent post-operative complications (adhesions, ileus, stricture at anastomosis site) Large Intestinal Strangulation Volvulus of ascending colon most common (lack of attachment to root of mesentery, only 1) May be secondary to changes in colonic motility and more common in broodmares just before/after parturition Degree of volvulus important - 270 degrees strangulating Acute colic (mild to moderate if non- strangulating but severe if strangulating) abdominal distension, +/- decreased GI sounds, no gastric reflux (unless LI distension occludes SI), CV compromise (if strangulating), LI distension with taught taeniae per rectum, serosanguinous peritoneal fluid (if strangulating) Rx - surgery and intensive medical therapy Prognosis - poor to guarded depending on degree of strangulation Large Intestinal Displacement Displacement of ascending colon most common (lack of attachment to root of mesentery) May be secondary to gas distension and displacement results in further non-strangulating distension Most common large colon displacements - Left dorsal (LLD) - ascending colon becomes displaced dorsally in the nephrosplenic space - Right dorsal (RDD) - pelvic flexure moves cranially and then to right of caecum (normally on left) Acute to chronic colic (mild to severe depending on distension) abdominal distension, +/- decreased GI sounds no gastric reflux minimal CV compromise LI distension (+/- abnormal location of LI) per rectum normal peritoneal fluid +/- ultrasonography for LDD (wont be able to see the kidney and spleen next to each other) treatment - LLD phenylephrine + lunging (contracts spleen, intestine slips off), GA + rolling, +/- surgery - RDD general medical Rx, +/- surgery Prognosis - good Intestinal Intussusception Can be jejuno-jejunal, jejuno-ileal, ileocaecal, caecocaecal or caecocolic Consequence of abnormal GI motility, +/- parasitism (tapeworms or small strongyles) May or may not be strangulating (depending on on how much the intestine goes in) Clinical signs dependent on site and severity, +/- able to identify on ultrasonography Rx-surgery Intra-Abdominal Adhesions Usually secondary to previous abdominal surgery (especially in foals), peritonitis (especially if fibrinous), intra-abdominal abscessation etc. May or may not be strangulating Clinical signs dependent on site and severity Rx - medical therapy if only mild colic, surgery if colic more severe or unmanageable medically Diarrhoea Common causes of acute diarrhoea in the adult horse Dietary indiscretion Grain overload Rapid dietary change (esp. low to high concentrate) Sand enteropathy Specific irritants/toxins (e.g. linseed and castor oils, heavy metals, toxic plants) Gastrointestinal parasitism Ascarids, large and small strongyles Larval cyathostomiasis foals: Strongyloides westeri and cryptosporidia Antimicrobial-associated Any antimicrobial can cause diarrhoea in adults horses! Due to dysbiosis Variable onset of diarrhoea in relation to treatment with antimicrobial drug May be transient or life-threatening! Acute salmonellosis Often associated with stress and antimicrobial therapy Highly contagious + zoonosis Diagnosis: faecal cultures and/or PCR - may need up to 6 consecutive cultures (intermittently shed in faeces) Antimicrobial therapy usually not indicated unless persistently severely neutropaenic - no evidence this speeds up recovery Clostridiosis Clostridium difficile/perfringens +/- Haemorrhagic diarrhoea Highly contagious Diagnosis by PCR for detection of clostridial toxins in faeces Treat with oral metronidazole Lawsonia intracellularis Proliferative protein-losing enteropathy of young horses (5-7 months ONLY) Diagnosis by severe hypoproteinaemia, thickened SI on ultrasonography, faecal PCR, serology, histopathology (sliver stain) Antimicrobial therapy (macrolide & rifampin or tetracyclines) Other Right dorsal colitis (NSAID toxicity) Peritonitis Stress Neorickettsia (Ehrlichia) risticii (Potomac Horse Fever) - exotic Grass sickness - exotic (europe, neurologic disease) Acute Diarrhoea (Foals) “Foal heat” diarrhea Dietary indiscretion (over-feeding) Peripartum asphyxia syndrome Antimicrobial-induced Lactose intolerance(?) Parasitic enteritis Viral enteritis Bacterial enteritis Chronic diarrhoea Chronic parasitism Chronic salmonellosis Lawsonia intracellularis infection Giardiasis(?) Peritonitis Sand enteropathy Inflammatory bowel disease Neoplasia Dietary sensitivity (abnormal VFA production)) ** Many cases of acute and chronic diarrhoea are idiopathic and will resolve (or not resolve) without a definitive diagnosis** should warn owners about this Lecture 13: dysphagia and weight loss Approach to a horse with dysphagia History Duration of dysphagia Previous episodes of dysphagia Other recent diseases and medications Normal diet and any dietary changes Appetite Nasal discharge Quidding (dropping food out mouth) Weight loss Dentistry Physical examination Signs of dysphagia (food coming out nostrils) Nasal discharge Quidding Vital signs (TPR) CV status (MMs and CRT, skin turgor, pulse quality, palpate extremities) Signs of aspiration pneumonia Oral disease Neurologic deficits (specifically surround CN deficits — swallowing related) Ancillary diagnostics NG intubation (must do if considering oesophageal obstruction) watch horse eat Oral examination Neurological examination URT endoscopy/oesopahgoscopy URT/oesophageal radiology (+/- contrast) Work up for aspiration pneumonia Oesophageal obstruction (“choke”) * EXAM QUESTION * main cause of dysphagia in horses Most commonly associated with the rapid ingestion of feed - usually at top and bottom of peaking order in group Nasal reflux of saliva and feed distress, retching, sweating, extended neck +/- palpable mass in neck Diagnosis passage of NGT - if you cannot pass tube could be obstruction +/- endoscopy and/or radiography As strated Treatment ↓ muscle prevent aspiration Sedation (relieve distress, relax oesophagus and lower head) ~ Pass NGT and lavage obstruction with water (keeping head lowered). NEVER OIL!!!!! +/- Systemic muscle relaxants, topical local anaesthetic General anaesthesia (+/- surgery) may be needed (cuffed tube in and repeat NG tube lavage) Supportive therapy (IV fluids) **Impaction must be relieved within 24 hours to avoid oesophageal ulceration and stricture** Prevention Feed small amounts frequently Avoid competition at feed time Rocks in feed tub to limit “bolting” feed Avoid offending feeds (individual dependent) Other Causes of Dysphagia Anatomic abnormalities cleft palate, subepiglottic cysts, retropharyngeal lymphadenopathy (e.g. Strangles), other URT masses, other oesophageal diseases Functional abnormalities primary neurologic disease (CN IX, X, XI, XII disease, botulism, tetanus) Approach to a horse with weight loss Pathophysiologic Mechanisms 1. Anorexia (usually disease-related) 2. Increased nutrient demands —> physiologic, pathologic 3. Protein-calorie malnutrition Severe weight loss is usually suggestive of chronic anorexia, increased nutrient demands or malnutrition/starvation Exception is in cases of severe disease processes such as acute colitis, acute pleuropneumonia, neoplasia — horses loss weight in short time period History Duration and severity of weight loss Does horse eat normally Owners estimate of amount of weight lost More than one horse affected Weight loss vs failure to gain weight Housing Appetite-↑,↓,normal “Occupation” Current diet Faecal consistency Dietary changes Deworming regimen Competition for feed Dentistry Other recent disease Physical Examination Estimation of body weight (BW) and BCS - Visual appraisal (inaccurate) - Weight tape - scales Thorough physical examination Appetite, prehension, mastication and deglutition Evidence of systemic disease Faecal examination (consistency, feed, sand, parasites) Estimation of Body Weight Visual appraisal (a.k.a. “guessing”) Inherently inaccurate! Weight tapes tape around horses girth Correlation between circumferance of girth and BW Less accurate in foals, ponies and horses with very high or low BCS Body condition score A scoring system to describe the “body condition” of an animal (NOT weight) Correlated with body fat content Australian (0-5) and American (1-9) equine body condition scoring systems Feed and pasture examination Quality and quantity of feed provided Competition with other animals Terrain and soil type (sand) Toxic plants (usually don’t eat unless nothing else to eat) Oral examination Dental abnormalities Other oral cavity diseases (e.g. masses, foreign bodies, inflammation) Routine Laboratory Diagnostics PCV/TPP - anaemia, dysproteinaemia CBC/fibrinogen/SAA - inflammatory processes Biochemistry - albumin/globulins, hepatic & renal parameters Urinalysis FEC Other Diagnostics Feed analysis or nutritional consultation (in large operations) Rectal examination, abdominocentesis Ultrasonography - abdomen and thorax Gastroscopy, malabsorption tests, coeliotomy Specialised laboratory diagnostics (usually following abnormalities on regular tests) MOST Common Causes of Weight Loss 1. Inadequate feed quantity or quality 2. Dental disease 3. Parasitism Inadequate Feed Quality and/or Quantity Increase quantity and/or quality of primary feed source (GRADUAL!) Supplement with calorie-rich feeds (GRADUAL!) Remove (if possible) any reasons for increased nutritional demands e.g. wean older foals Nutritional education Reassess body condition/weight in 1-2 months Dental Disease Correct dental abnormalities - sharp points, hooks, ramps, wave mouth, missing molar teeth (“step mouth”) - may take several attempts to correct severe abnormalities and require advanced dental equipment Institute prophylactic dental care Reassess body condition/weight in 1-2 months Parasitism Most commonly a result of high internal parasite load (e.g. cyathostomes) Severe ectoparasitism Value of FEC (0 FEC does NOT rule out parasitism) Widespread BZ resistance by cyathostomes Some resistance to ivermectin by ascarids Treatment “Larvicidal” deworming on 1-2 occasions (moxidectin, extralabel fenbendazole) Treatment for tapeworms (praziquantel) Monitor faeces for gross parasites Monitor FEC Institute appropriate parasite control regimen Reassess body condition/weight in 1-2 months Less Common Causes of Weight Loss 1. Inflammatory bowel disease - granulomatous or eosinophilic entero-typhlo-colitis 2. Neoplasia 3. Pituitary pars intermedia dysfunction Inflammatory Bowel Disease Chronic, idiopathic inflammatory disease Often seen in young horses Variable appetite, +/- diarrhoea, protein losing enteropathy and oedema Dx - lab results, rectal examination, abnormal glucose/xylose absorption (SI), biopsies, necropsy Rx - +/- corticosteroids Prognosis - poor Neoplasia Lymphosarcoma Squamous cell carcinoma Malignant melanoma Other carcinomas Haemangiosarcoma Lymphosarcoma Most common non-cutaneous neoplasm of equids Four anatomic syndromes based on location of primary mass (can overlap) - Alimentary (lymph nodes and/or intestinal tract) - Mediastinal (lymph nodes and/or thymus) - Cutaneous - Multicentric NO age predilection - common in young horses Variable clinical signs depending on site of lesion Dx - laboratory results (leukaemia very rare), fluid cytology, rectal examination, ultrasonography, biopsy, coeliotomy, necropsy Rx - +/- transient response to corticosteroids, some reports of other chemotherapy limited Prognosis grave, except for cutaneous (if only masses in skin - long term survival) Pituitary Pars Intermedia Dysfunction Other Causes of Weight Loss Any chronic disease - liver, GI, CRF, CHF, LRT, peritonitis Abscessation - thoracic or abdominal Chronic dysphagia Grass sickness/EMND (exotic)