Equine Acute and Chronic Diarrhoea PDF

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Anna Hammond...

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Equine Acute and Chronic Diarrhoea Logically approach diarrhoea cases Appropriate examination and testing Formulating a list of differential diagnoses. Supportive treatment for diarrhoea cases Know when emergency treatment is required Mechanisms of Diarrhoea - Most fluid entering GI tract reabsorbed in LI - Up to 100 L/day can be lost → extreme dehydration - Inflammation of the bowel = colitis → reduced ability of the LI wall to reabsorb + increased secretion by the LI wall + decreased transit time. Diagnostic Approach - History - Age - Acute vs Chronic - Diet changes - Worming - Single or multiple affected - NSAID or AB usage - Ddx - Chronic Diarrhoea - G = Granulomatous Bowel Disease - I = Bacterial (e.g. Chronic Salmonellosis), Parasitic (e.g. Cyathostomiasis), Inflammatory (e.g. Sand) - A = Inflammatory & Granulomatous Bowel Diseases - N = Neoplasia (e.g. Lymphoma) - C = Chemical and Toxic - e.g. Iatrogenic NSAID use → Right Dorsal Colitis - Acute Diarrhoea - I = Bacterial (e.g. Salmonella, Clostridial toxin, Rhodococcus), Parasitic (e.g. Cyathostomiasis), Viral (e.g. Rotavirus) - N = Nutritional - sudden diet changes - I = Idiopathic - C = Chemical and Toxic - e.g. Iatrogenic NSAID or AB - Testing - Effect of D+ on the Individual - Dehydration (Acute D+) - HR, PCV, TP (submandibular/ventral oedema) - Endotoxaemia (Acute D+) - Clinical exam, HR, mms = red/purple - Inflammation - Temperature

- Colic + Fever → Colitis or Peritonitis → Abdominocentesis Protein loss - TP + Albumin → ventral oedema? - Electrolytes (Acute D+) and Acid-Base (Acute D+) - Test once rehydrated as Hypokalaemia/chloraemia/natraemic will likely resolve - Detecting the Cause - Faecal Sample - Bacteriology (3 serial samples for Salmonella) - Clostridial toxins - FEC - Biopsy - IBD, Neoplasia, Salmonella culture, Encysted Cyathostomes - Rectal = cheap, easy, low risk - Intestinal via laparoscopy (standing) or laparotomy (uGA) - Laparotomy has 3 month recovery time but easier for LI biopsy and inspection of abdomen - Abdominoparacentesis - Neoplasia - ¼ lymphoma and ¾ SCC seed - IBD - inflammatory cells - Abdominal US - Thickened intestinal wall (black line of oedema between layers) IBD, Right dorsal colitis, Neoplasia Treatment - General - Acute = Supportive - Dehydration - IVFT = Dehydration + Ongoing losses + Maintenance (2 ml/kg/hr) - Monitor and adjust - Electrolyte Imbalance - Feed - Spiked fluid bags (Hartmann’s + KCl) - Acid-Base - D+ can cause Acidaemia - Hydrate first then if needed give Bicarbonate IV - Hypoproteinaemia - Plasma infusion (may need to repeat) = 1 L/100 kg - Very expensive - Endotoxaemia - Flunixin - risk of Colitis - Polymyxin B binds LPS - Must treat to avoid Laminitis - icing feet? - Colic - Flunixin - Opioids (short duration), Spasmolytics -

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Bacteraemia - ABs - risk colitis - Monitor for Thrombophlebitis - Encourage Blood Flow to Colon Wall - PG agonists - Sucralfate + Misoprostol PO (half hour gap after Sucralfate) - Bio-sponge - binding of toxins - Yeasacc - raised Gut pH - Nursing = clean, Vaseline (prevent scald), feeding Treatment - Specific - Bacterial - Salmonella enterica - 4 Clinical Syndromes - Inapparent infection - Latent/carrier state - Depression, Fever, Anorexia, Neutropenia w/o D+ or Colic - Acute Enterocolitis w/ D+ - Septicaemia +/- D+ - Transmission = faeco-oral - Persists in the environment - Carriers show disease if immunocompromised - Risk Nosocomial or Zoonotic infection - CS Enterocolitis = Fever, Anorexia → Endotoxaemia → Shock → D+ → Dehydration, Mild-moderate Colic + PLE, Early neutropenia, Ulcers - Dx = CS + Culture (rectal biopsy best) - Need aggressive Tx - High risk complications - e.g. Laminitis, Carrier status, Chronic salmonellosis (poor prognosis) - Clostridia - Normal gut flora → trigger = AB - Dx = Toxins on faecal sampling (ELISA), US - Gas bubbles in gut wall - Prognosis = poor - Lawsonia intracellularis - Faeco-oral transmission - Obligate intracellular pathogen → proliferative enteropathy of SI → altered absorption of nutrients + altered fluid secretion (disruption of villus architecture) + altered maturation of epithelial cells - CS = D+, severe weight loss, PLE, ill thrift, peripheral oedema, colic - Most commonly weaning foals (4-6 months old) - Clin Path = Hypoalbuminaemia, Hyperfibrinogenemia, Anaemia - Abdominal US = Thick, oedematous intestinal wall

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Dx = Serology + Faecal PCR, definitive = Histopath Tx = Supportive - Plasma transfusion, Doxycycline for 4-6 weeks

Parasitic - Cyathostomiasis - Migration of L4 through mucosa of LI where they encyst (Hypobiosis) → Mass emergence (Spring) - Large burden → inflammation → D+ + PLE - CS = Acute D+ (becoming chronic), Weight loss, Ventral oedema, Intermittent pyrexia and colic - Trigger = recent deworming? - Dx = Larvae in faeces? Rectal biopsy for encysted larvae - Tx = Worm with Moxidectin (less inflammation than Fenbendazole) + Corticosteroids (e.g. Dexamethasone) Toxic/Iatrogenic - NSAID - Gastric ulceration, Right dorsal colitis - CS = Anorexia, Lethargy, Colic, D+ (acute or chronic), PLE → ventral oedema - Dx = Thick colon wall on US - Tx = PG analogues, Stop NSAID (opioid + buscopan for analgesia) - AB induced - Penicillin? - Dams ingesting Erythromycin via foal → fatal colitis due to disruption of normal flora and clostridial overgrowth - Tx = Metronidazole Inflammatory Bowel Disease - Chronic with Acute episodes - CS = Weight loss (SI), D+ (LI) - Dx = US - thickened gut wall, Inflammatory cells in peritoneal fluid, Biopsy best - Tx = Corticosteroids, Resection if localised, Short fibre diet, Yeasacc Idiopathic - Symptomatic tx

Foals - Foal Heat D+ - Mild, self-limiting - 5-14 days old - Rotavirus - Most common D+ cause in young foals - Dx = Virus in faeces - Control = stable hygiene + vaccination of dam - Self-limiting - Bacterial

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< 2 weeks old - underlying FPT and Sepsis > 3 months = Rhodococcus...