Urinary Tract Diseases in Horses Notes PDF

**[L2→ URINARY TRACT DISEASES IN HORSES]** **[Common presenting signs of kidney disease]** - PU/ PD - Oliguria/ anuria (decreased urine output) - May persist despite IVFT - Lethargy, inappetence - poor performance - No CS **[ACUTE RENAL FAILURE/ ACUTE KIDNEY FAILURE]** **Pat...

**[L2→ URINARY TRACT DISEASES IN HORSES]** **[Common presenting signs of kidney disease]** - PU/ PD - Oliguria/ anuria (decreased urine output) - May persist despite IVFT - Lethargy, inappetence - poor performance - No CS **[ACUTE RENAL FAILURE/ ACUTE KIDNEY FAILURE]** **Pathophysiology** - Most AKI due to acute tubular necrosis (ATN) - Death and sloughing of tubular epithelial cells - Obstruct tubular lumen→ no urine output form blocked nephrons - 20% of total renal blood flow goes to the medulla, 80% to the cortex - ATN caused by toxic insult (including drugs - Different specific toxic actions - PCT/ Cortex most affected (most blood flow here) - ATN caused by ischemia - Loop of henle /medulla most affected (least blood flow in this area) **History** - Most cases→ Administration nephrotoxic drugs - Aminoglycosides - NSAIDs - oxytetracyclines - Primary disease causing renal hypoperfusion or ischaemia - Often have kidney disease with combination of these factors in the history - Combination of these - Exposure to other renal toxins [Aminoglycosides] - Toxicosis almost always due to repeated administration - Frequent dosing more than single high doses - Uptake of aminoglycoside cations is a saturation process - Single large dose should be less nephrotoxic - Prolonged administration [NSAIDs] - Excessive doses, prolonged treatment or both - If combine with Hypovolaemic patients → risk of acute tubular necrosis - Concurrent GI ulceration - Manifests in the medullary region→ Medullary crest necrosis - Decrease production of all the happy prostaglandins that promote vasodilation (PGE~2~, PGI~2~)= Loss of vasodilation - Have an increase in renal vascular resistance→ accrue tubular necrosis - If giving to horses with pre-existing renal issues - Fever - Hypovolaemia - Given NSAIDs→ make ischemia in kidneys worse - Careful giving these in volume depleted horses [Other causes of acute renal toxicosis] - Pigment nephropathy (Haemoglobin, Myoglobin) - Tubular obstruction - Direct toxic effect of pigments - Heavy metals - Acorn poisoning - Other drugs - Oxytetracycline - Foals with flexural limb deformities→ careful administering high doses to these guys - Polymyxin B (antimicrobial stewardship!) - Vasomotor nephropathy - Renal artery constriction→ reduced blood flow to kidneys→ acute Ischaemic necrosis - History - Biochemistry - Increased creatinine (most reliable biochemistry indicator) - Herbivores rely more on creatinine → Not confounded by dietary urea & fermentation by microbes & muscle metabolism like BUN - Increased BUN (beware confounding factors) - Urinalysis - USG - decreased ability for kidneys to concentrate urine - Dipstick often normal - Even if have AKI but still worth doing - Sediment - Casts (often not seen -- alkaline pH) - Cells - Pigments (Hb, Mb) - Haematuria - IV fluids - Main stay of treatment - Correct electrolyte and acid-base abnormalities - Determine polyuria/oliguria/anuria - Often have polyuria and will be able to clear fluid - Oedema risk if oliguric/anuric - Cannot clear the fluid - If oliguric/anuric after 12-24 h IVFT → furosemide - May be useful to get urine flow going again - PCV/ TP - Bodyweight - No weight gain after initial rehydration - Urine output - Hard to measure, May just observe how wet the stall is - USG - BP - CVP - Central venous pressure not commonly done anymore - May do if worried about fluid overload - Creatinine +/- BUN - Want to know you are improving the kidney function by getting rid of the excess creatinine **Prevention of renal failure/ acute kidney injury** - Close monitoring of patients receiving nephrotoxic medications - Creatinine - GGT: creatanine ratio - Therapeutic drug monitoring (aminoglycosides) - 5-7 days of aminoglycosides - Careful use of oxytet in foals - Slow administration - Administer with IV fluid - Don't administer on consecutive days - Give the kidneys time to clear it before you give them more - Avoid exposure to toxins **[CHRONIC RENAL FAILURE/ CHRONIC KIDNEY DISEASE]** - Irreversible and progressive decline in glomerular filtration rate - Glomerular or tubulointerstitial in origin (One often leads to the other) [Common presenting complaints/ history ] - Weight loss - PU/PD - Poor performance - History of previous AKI or admin of nephrotoxic drugs [Physical exam] - Non-speciifc findings - Dental tartar (esp canine teeth in males) - Mild ventral oedema associated with excess sodium retention **CKD- Clinical pathology** [Plasma] - Azotaemia - Hypercalcaemia - Already excrete a lot of calcium in their urine as calcium carbonate crystals in normal horses - If can't do this as their kidneys are not working normal may end up with excess calcium in the plasma - Horses with high calcium diet are also at risk of this - +/- Hypermagnesemia - Acid-base normal unless end-stage - Isosthenuria - (Proteinuria -- glomerular disease) - (Haematuria, pyuria -- pyelonephritis) - Less common in standard kidney disease - Urine clear -- lack of crystals, mucous - Often opaque due to mucous & crystals→ may look unusually clear **Causes of CKD** [Chronic interstitial nephritis ] - Sequela to acute tubular necrosis or other kidney disease - May have occurred years ago and appear to have recovered but then down the track have kidney disease - Fibrosis [Pyelonephritis] - Rare - Often concurrent Nephroliths/ureteroliths - Risk factors - Sluggish urine flow, LUT disease - Uni- or bilateral [Proliferative glomerulonephritis] - Type III hypersensitivity - Immune complex deposition in glomerular membranes→ CKD Others - Amyloidosis - Polycystic kidneys - Congenital renal dysplasia - Neoplasia - Primary renal neoplasia is quit **Diagnosis of CKD** - Biochemistry, urinalysis - Ultrasound - Biopsy - Always US guided - Always right so don't have to go through the spleen - Can do this if you have to but want to avoid due to risk of haemorrhage - Cystoscopy, C&S (pyelonephritis) - Looking for difference in urine flow coming from each ureter **Treatment/ Management** - Acute exacerbation of chronic disease - Stable CKD - Want to ensure have adequate hydration - Salt supplementation if needed (NOT if oedema) - Diet -- good quality, avoid excess protein - Don't want to restrict protein as need this for good body weight but don't want to give them excess protein - Monitoring - End stage - Maintain appetite, caloric intake - Try to prevent them from losing too much weight - Pyelonephritis - Antimicrobials -- prolonged course based on C&S - Use ones excreted in the urine so have good conc. in the kidneys - Nephrectomy (if unilateral) - May be an option in referral hospital **[GROSS HAEMATURIA]** - Idiopathic renal haematuria - Renal calculi - Neoplasia - Kidneys - Bladder - Cystic calculi - Urethral haemorrhage **Diagnosis of gross haematuria** - Haematology and biochemistry - Do you have functional kidneys - Urinalysis - Presence of blood in the urine - Specific gravity - Ultrasound - Cystoscopy → Determine where the haematuria is coming from **[IDIOPATHIC RENAL HAMEATURIA]** - Sudden onset gross haematuria - Many breeds effected (Arabians overrepresented) - Often unilateral, Can be bilateral - Signs of blood loss -- anaemia, pale membranes - Due to how severe the haemorrhage can be - Haemorrhage may be life threatening - Usually NOT azotaemic - Often have at least one functional kidney - May see haematomas on the effected kidneys - Treatment supportive - Relatively rare - Prognosis usually poor [Kidneys] - Adenocarcinoma/Renal cell carcinoma - (Nephroblastoma) - Secondary - Adenoma, Lymphosarcoma, Hemangiosarcoma, Melanoma (greys) [Bladder] - Squamous cell carcinoma - Transitional cell carcinoma - Usually single, large, spiculated stones - Calcium carbonate - Bacteria often present but role unclear - Occurrence rare in horses - Haematuria after exercise - Stranguria, dysuria, pollakiuria, incontinence also occur - May also have poor performance [Diagnosis] - Palpation per rectum - Sometimes possible - Cystoscopy - US per rectum [ ] [Treatment] - Surgical removal - Too big to remove any other way - Fragmentation and removal - Through urethra in mares, perianal urethrostomy in males - Concern for recurrence with fragmentation method due to possibly leaving bits behind [Prevention] - Grass hay diet recommended - Reduce legumes - Helps to reduce calcium and calcium carbonate in the urine - Urinary acidification - try with ammonium chloride→ h hydrogen ion excretion in the urine - Increase water consumption by adding some salt to their diet **[URETHRAL HAEMORRHAGE]** - Male horses - Present most commonly as gross haematuria at end urination, end ejaculation (also haemospermia) - Increase pressure in the tissue of the penis→ blood passed through tear in urethra that ends up in the urine - Normal voiding of urine & "squirts" of frank blood at end - Differentiate from pigment-uria→ expect discoloured urine to be present in the whole stream - QH & QHX breeds overrepresented - Can be seen in any breed - Breeding stallions at higher risk [Diagnosis ] - Endoscopy - Bleeding stallion→ sexual rest - Gelding→ temporary urostomy to urinate through to take pressure off **[URINARY INCONTINENCE]** - Bladder paralysis - Loss of detrusor function - Often due to lower motor neuron disease - Many causes (e.g. EHV-1, EPM (N and S America), trauma) - Sabulous urolithiasis common consequence - Have very fine silty sludgy material built up in the bladder - May have concurrent infection [Management] - Repeatedly empty the bladder - Most don't do well in the long run **[LOWER URINARY TRACT DISEASE IN FOALS→ Bladder Rupture]** - Urinary bladder rupture= most commonly seen urinary issue in foals - Often the dorsal bladder wall that ruptures - Otherwise healthy foal - Healthy first few days bouncing around, feeding etc and then after 2 days old becomes unwell - Sick foal - Recumbent - Not emptying bladder [Clinical signs] - Dull, lethargic, stranguria - Loss of interest in nursing - Abdominal distension - Tail flagging -\> Due to being uncomfortable [Diagnosis] - CS - Abdominal ultrasound - large volume free peritoneal fluid - Loops if SI and mesentery - +/- sites of bladder rupture - Plasma electrolytes: - Hyponatraemia - Hypochloraemia - Hyperkalaemia - All in association with azotaemia - Can be difficult to detect in foals that have been on IV fluids - Get these changes as the foals diet is milk→ potassium rich, sodium poor → Foals can't excrete the potassium as bladder is ruptured→ more potassium in the body - ECG if severe hyperkalaemia - Azotaemia (post-renal) - Peritoneal fluid analysis - Peritoneal fluid creat ≥ 2x plasma creatanine - (Contrast radiography) - Used to be used before US, not as commonly done anymore [Treatment] - Surgical repair - Don't heal themselves - Often only option - Stabilise prior to anaesthesia - Correct electrolyte abnormalities (esp. HyperK, care with sodium) - Hartman's is the best fluid choice→ Safer - Address cardiovascular compromise - Address any underlying disease (sepsis) - Peritoneal drainage may be effective until systemically stable - If have urine drainage don't need to rush them to surgery - Manage any FPT, sepsis [Addressing hyperkalaemia] - IV fluids - Care with longstanding (\> 24 hours) hyponatraemia \< 120 mmol/L - Need to correct sodium slowly→ Want to ensure we don't have osmotic demyelination syndrome in the brain - Dextrose in IV fluids - Creates an endogenous insulin response→ drives K+ intracellularly - If severe hyperkalaemia (\> 8 mmol/L) and/or ECG changes are present: - Calcium gluconate (23% solution) - 0.5-1 ml/kg in first 500 ml of IV fluids given over 10 min - Helps restore normal gradient between resting membrane potential and threshold - Exogenous insulin - 0.1-0.2 IU/kg SC or IV + dextrose infusion (4-8 mg/kg/min) - Drives potassium intracellularly **[L6→ COLIC BY SIGNALMENT]** **[Why horses are frequently effected by colic]** - Hind gut fermenter - Very large fermentative vat - Unable to eructate from the vat - Domestication - Changed diet→ ↑Grain - Changed use/ housing/ management - Poor gastro-intestinal tract design - U turns (pelvic flexure), bottlenecks (pelvic flexure, caecocolic valve), freely movable intestines (mesentery) - As distension or filling changes→ likely chance of movement causing problems **[Causes of abdominal pain in horses]** **Gastrointestinal pain** - Stomach, small intestine, large colon, small colon, rectum - Abnormal gas production - Obstruction - Functional: impaired motility of GI tract - Physical - Intraluminal - Feed Impaction -- conglomeration of dehydrated ingesta - Foreign material - Extraluminal - 'Kinked pipe' → Volvulus, lipoma [Ischemia ] - Strangulation - Extraluminal obstruction [Inflammation] - Enteritis - Peritonitis **[Colic by signalment ]** - Age - Breed - Arabian: Enteroliths in large intestine - Miniature pony: Faecoliths small colon - Sex - Female: uterine torsion, ovarian disease, pregnancy - Gelding vs. Stallion -- testicular torsion, scrotal hernia - Colour - Overo lethal white syndrome (ileocolonic aganglionosis) - Reproductive status (pregnant, multiparous) - Uterine torsion in late gestation - colon displacement/ torsion post partum **[Colic presentations common by age ]** - Neonates - First manure: meconium impaction - Congenital abnormalities/atresia - Immature body systems - prone to infections - Weanlings\...(months old) - Parasitic problems - Ascarid impactions - Intussusception - Young adult: - Less specific disease processes - More surgical and medical - Teens to Older animals - Neoplasia- that takes time to develop - Rare - Benign lipoma most common - Impactions due to dental problems - Effecting feeding **Relevant history→ foals** - Age (couple days vs weeks change Ddx) - Normal foaling? - Hypoxic event now effecting GI tract - Progression of signs - Nursing? - Sick foals go off milk very quickly - Previous analgesics? - Often not given in foals but good to ask - Neonate: - Passed meconium? - Have they been given an enema? - Urinated? → Ddx ruptured bladder **[Interpretation of pain in foals]** +-----------------------------------+-----------------------------------+ | **Mild** | **Severe** | +===================================+===================================+ | - Restlessness | - Lying down/ on back or | | | rolling | | - Attempts to pass manure | | | | - Bruxism/ reflux from nares | | - Tail swishing | | | | - Sweating | | - Straining to urinate/ | | | frequent urination | - (lack of) response to | | | analgesia | | - Not nursing: Mare runs milk | | | | - Mare runs milk | +-----------------------------------+-----------------------------------+ **[Physical exam ]** - Normal foal parameters differ from adults - Resting HR & RR higher - HR 100 in first 24 hours - Higher 'normal' temp→ Up to 39°C [Signs suggestive of possible surgical lesion] - Tachycardia \>120bpm - Absence of fever - +/- abdominal distension - Inability to control pain - Supportive ultrasound findings **6- 24 hours → First day of life** - Meconium impactions - Often all pass in first 24 hours - Ileus assoc. with hypoxic ischemic syndrome/ enteritis - Seen with difficult foaling - Enteritis→ ileus Less commonly - Congenital atresia- (colon, rectum, anus) - Lethal white foals: ileocaecal aganglionosis - Genetic make up→ very uncommon - Foals are non-viable **[MECONIUM IMPACTION]** Meconium→ made up of glandular secretions from GI tract, amniotic fluid & cellular debris - Should be passed by 24-36 hrs of age [Higher risk foals: septic ] - Hypomotility induced by hypoglycaemia & sympathetic drive of the foal - endogenous & from drugs administered - If presented with foal with meconium impaction, look for signs of systemic illness - Want to treat as early as possible - More common in colts (narrow pelvic canal) **[LETHAL WHITE FOAL SYNDROME]** - Primarily white foals - Parentage: (frame) overo - White face/blue eyes - DNA test available - Lack myenteric innervation from ileum and through large intestine - Colon narrow/ absent - Severe irreversible ileus - Meconium and gas distension **Foals 3-5 months with colic** **[ASCARID IMPACTION]** - Hx of dewormed a week prior - Large worm 'kill' resulting in physical obstruction of the small intetsine - Often have a very Poor prognosis compared to other types of surgical colic (25%) - Ascarids release toxins - Inflammation from surgery and worms - Prolonged ileus common - High risk adhesions - Foals are often unthrifty **[INTUSSUSCEPTION (UP TO 2 YEARS)]** - Telescoping' of bowel into itself - Target lesion on US - Thought may be due to worm burden effecting motility of GI tract - Can cause partial to complete obstruction - CS can be progressive - Intermittent low-grade pain with incomplete obstruction & then more violent severe colic signs with complete obstruction - Gradual necrosis of internal portion of gut - Common locations - Jejunojejunal - Ileocaecal - Caecocolic **Foals 6 months with colic** **[GASTRODUODENAL ULCERATION]** - Ulceration more clinically signif. in foals - Bowel can stricture during healing causing outflow obstruction after initial ulceration - Stricture → colic signs - Physiologic stress, Hypoxia, illness - Decrease mucosal defences possibly due to reduction in mucosal blood flow - Long time between feeds - Prolonged exposure to acidic pH - NSAID - Inhibition of protective prostaglandins [Dx] - 1m gastroscope after 2hr fasting - Reflux/ duodenal & gastric distension [Effects] - Can be life threatening - Peritonitis due to gastric rupture→ peritonitis→ Death - Obstruction due to stricture [Typical presentation] - 2-5mo weanling - History of prior illness - Depression & intermittent nursing - low grade colic - Bruxism, ptyalism, dorsal recumbency **Older animals** - Lesions that take time to develop (\>15yrs) - Can be very stoic - Have very subtle signs of colic - Benign: Lipomas - Form on mesentery of the SI→ strangulate portion of small intestine - Malignant neoplasia uncommon - (adenocarcinoma/lymphoma\*) [Prognosis?] - \>16y no difference in surgical survival rates - May take longer to bounce back **[POOR DENTITION]** - Can lead to impactions - Donkeys live into 50's - Metabolize NSAIDs faster - Dose more frequently - Beware masking signs **Sex influencing Ddx** **Stallions** - Can get enlargement of the scrotum **[TESTICULAR TORSION]** - Enlargement of the tetsicle - Spermatic cord torses around itself casuing vascular compromise - Extremely painful - Signs of abdominal pain **[HERNIATION OF INTESTINAL TRACT]** - Often through inguinal ring and fills up scrotal sac - Dx→ placing US on scrotum - See SI loops filling scrotal sac **[Inguinal herniation- adult vs neonate]** [Adults] - Surgical emergency - Once intestine has herniated through the inguinal ring and fills up scrotal sac→ can't return to the abdominal cavity - Becomes distended, oedematous [Neonates] - Inguinal ring is larger - SI comes through & can get back through - Not an emergency - Can manage conservatively by repeatedly reducing herniation over a few days - As foals mature, inguinal ring becomes smaller & doesn't allow intestines to come through inguinal ring [Indications for surgery] - All adults (emergency) - Foals only if; - Non reducible, heat, pain - Subcutaneous - Increasing size/ client frustration - Maiden mares - May have low grade colic due to foal moving around - Foaling wants out→ foaling vs abortion - Running milk, Cervix open, Placental health? - Uterus twisted - broad ligaments cross one another - Can fix surgically or through rolling - Need to be certain of Dx for rolling **Broodmares; post foaling** - Retained foetal Membranes - hours post foaling, sometimes low- grade colic - Rupture of uterine artery - up to 48hrs post foaling - Can bleed out and die due to this - control bleed, allow clot formation - Tear of uterine wall - 2-3 days post foaling - Signs of peritonitis **[LARGE COLON VOLVULUS]** - Anytime in post foaling period - More room to move around - Most severe colic in horses - Violent pain - -Artery Haemorrhage / GI Ischemia [Hendra: ] - Northern NSW or QLD, unvaccinated - 100% seropositive euthanased - no specific signs - Human health risk [Enteroliths] - NSW - Lucerne/ little turnout - Mineral concretions ['Sand colic'] - Horses living on lots of sand→ impaction ['Swim colic' ] - (violent) Colic 30mins after swimming - Small proportion surgical **[L7→ PARASITIC MANAGEMENT]** **[Introduction ]** - Anthelmintic over-use due to promotion of rotational deworming → Resistance - Don't want to do rotational deworming [Main disease-causing culprits] - Small strongyles (cyathostomins) - Ascarids (Parascaris spp; foals) - Tapeworms (Cestodes; Anoplocephala spp.) [Resistance] - Benzimidazoles (54-98% farms) - Pyrantel (41% farms) - Macrocyclic lactones (0% farms) **[SMALL STRONGYLES]** - Adults non-pathogenic - Not worried about adults - Encysted larvae are the main concern - Severe colitis - Hypoproteinaemic - Colic & Diarrhoea - Horses Ingest the L3 larvae from the pasture - Early L3 larvae can encyst in wall of the colon - When the conditions are optimal, they can come out all at once→ Mass emergence **Mass emergence** - Late winter to early spring - Late summer to early autumn - Severe weight loss, diarrhoea, hypoproteinaemia - Pass large numbers larvae/ adults in faeces **[CESTODES]** - Tape worms attach them self to the ileo-caecal valves - Cause colic in horses - Can be hard to diagnosis - Faecal flotation looking for proglottid passed out in faeces - No acquired immunity develops  **OTHER GI PARASITES→ mild disease** [Large strongyles] - Effective prevention in place - Not commonly seen [Strongyloides westerii] - Migrates to mammary gland in mare and is ingested by the foal - Can cause diarrhoea in young foals - Often self limiting [Oxyuris spp. (pinworms)] - Hang around at the anus and deposit eggs - Make horses have itchy bums [Gasterophilus spp. (bots)] - Larvae of the bot fly - Hang out in the stomach - Can cause some focal ulceration where they attach but often not severe disease [Ascarids (foals)] - Can cause severe disease in foals **[AVAILABLE ANTHELMINTICS]** **[ANTHELMINTIC RESISTANCE]** - Constant exposure to anthelmintics - Constant use that results in larval killing - Parasites retention of resistance genes **[SELECTIVE DEWORMING]** → ADULTS ONLY NOT FOR FOALS - Used for the prevention of anthelmintic resistance in small strongyles - Need to think about foals differently [Acknowledge the problem] - Convince clients resistance is a problem - Accept that completely parasite-free horses are neither possible nor desirable - Need horses to have some worms - Save the refugia→ Worms not resistant **Goals of selective deworming** - Prevent parasitic disease - Reduce pasture contamination - Preserve refugia = prevent resistance **Refugia? Where?** → Worms that don't see anthelmintics - In horses that don't get dewormed - Encysted larvae present when dewormed with anthelmintics that don't kill larvae - In the environment at the time of deworming **How do we preserve the refugia?** → Perform faecal egg counts - Once we know how many eggs are being shed→ only deworm the high shedders - +/- some moderate shedders [Interpreting FEC results] - Low shedders: less than 150 EPG - Moderate shedders: 150-500 EPG - High shedders: over 500 EPG **How to know is farm already has resistance?** - Perform FECRTs (on at least 6 horses) - When beginning selective deworming program - Every 2-3 years afterwards [How to do a faecal egg count reduction test] - Take a faecal sample from the horse - Faecal egg count - Deworm it - 14 days later take another faecal egg count - \>90% reduction → no significant resistance - 80-90% reduction → suspect resistance - \ - Expect better from them - \