Internal medicine cases

Case 1

• 6yo Appaloosa gelding wouldn't come into barn for feeding time.
• Appeared normal prior to that time, no recent history of injury, illness, medication. Next day owner noticed left head tilt and ataxia.
• Hospital examination- severe left-sided head tilt, base wide stance and severe balance loss. Horizontal nystagmus with a quick phase to the right was noted.
• Ventral stabismus in right eye.
• No evidence of depression, limb weakness or facial nerve abnormality.
• Based on age, acute onset of clinical signs- what would be the top differential diagnoses?
• How can it be determined if the vestibular dysfunction is central or peripheral?
• What diagnostics should be performed?
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Case 1 answers

• DDx- Trauma, temporohyoid osteoarthropathy (THO), equine protozoal myeloencephalitis (EPM)
• Peripheral and central vestibular disease- loss of balance, asymmetric ataxia, head tilt towards side of lesion (except paradoxical vestibular disease - head tilt contralateral ). Central vestibular disease- upper motor neuron proprioceptive deficits, weakness, depression. Nystagmus- horizontal or rotary--> fast phase opposite the side of the lesion (some central cases direction may change with different head positions or fast phase towards lesion)--> C1 spinal cord disease- signs of vestibular disease via damage to secondary spinovestibular tracts
• Diagnostics - Endoscopy of guttural pouch: normal. Collection of CSF: normal (EPM - titer was a weak positive on Western blot), CBC: normal except mild leukocytosis. Radiographs and/ or CT scan: declined by owner.
• Follow up/ discussion
• NSAIDs and DMSO- given IV and oral trimethoprim sulfa initiated. Ponazuril for EPM for 9 days, no improvement. Owners elected for euthansia
• Post mortem diagnosis: Aspergillus infection of left tympanic bulla. Infectious otitis media/interna - rare cause of peripheral vestibular disease- frequently blamed for cause of THO, infection rarely documented. Staphylococcus aureus- most common bacteria isolated
• Fungal infections of tympanic bullae- rare in equids.
• Systemic tx of Aspergillus: IV amphotercin B (limited- nephrotoxicity/ thrombophlebitis, some resistant strains) or oral itraconazole, fluconazole (well absorbed orally) or voriconazole (best bioavailabity, low toxicity, best efficacy against several strains, expensive).

Case 1 pictures/ answers

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• Legenda: Aspergillus infection in left tympanic bulla
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• Legenda: Cytology of aspergillus fungi

Case 2

• 8yo Thoroughbred gelding developed acute anorexia, fever (39.6 C).
• Winter and snow on pasture. No recent shipping, exposure to other horses or other typical risk factors for infectious diseases. Good deworming history. Had similar complaint in spring 5 yrs earlier- Actinobacillus spp peritonitis was confirmed and treated successfully. Reported to have been in good health since that time.
• Presentation- PE unremarkable had anorexia, fever, mild tachycardia, absence of gut sounds.
• Based on hx of case, w/o ultrasound in the field - what diagnostic procedures should be performed?
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Case 2 answers

• Diagnostic procedures - CBC and peritoneal tap.
• Follow up/ discussion
• CBC- mild neutrophilia w/o left shift. Fibrinogen 3g/l.
• Peritoneal fluid- dark orange, TP 4.7g/dl, 220,00 nucleated cell/ul (mainly degenerated neutrophils).
• No infectious agents seen.
• Culture- Actinobacillus equuli haemolyticus. Sensitive to ampicillin, aminoglycosides, cephalosporins, fluroquinolones and tetracyclines; resistant to trimethoprim sulfa and penicillin.
• Actinobacillus peritonitis- not rare in otherwise healthy horses. Occurs spontaneously in adults (9month old foals have been affected). Clinical signs- lethargy, depression, mild colic, anorexia and fever. Sensitive to most antibiotics. Causes- migrating parasites/ foreign bodies have been implicated.
• Pleuritis, pericarditis, and/or meningitis- can be associated with peritonitis.
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Case 3

• 15yo Appendix mare - intermitten bilateral epistaxis 5 days duration.
• PE- tachycardia 60bpm, marked swelling of both left cranial neck and left hindlimb. Mare 1/5 lame on LHL despite swelling. Jugular veins- normal on visual examination and palpation. Normal airflow through the nostrils and no petchiations or nasal discharge seen.
• Endoscopy performed.
• Platelet count was 13,000 cells/ul. PT and Partial thomboplastin times were normal. PCV 22%, TP 5.5mg/dl. All other CBC/ serum biochemistry was normal - mild increase in muscle enzymes (CK 888U/L, AST 720 U/L.
• Coggins test for equine infectious anaemia- negative, no history of prior drug administration within the past 3 months.
• What question should be asked regarding the swelling of the LHL and neck?
• Are the swellings most likely septic or non-septic?
• List some DDx for intermittent bilateral epistaxis
• What diagnostic test should be chosen next?
• Severe thrombocytopenia, no evidence of infectious disease/ drugs - which general type of disease process would be the top differential?
• What diagnostic test should be next?
• Further diagnostics to help evaluate the thrombocytopenia more specifically?
• Radiography of the lungs were performed to look for any metastases- interpretation?
• Most common neoplasm to invade muscle and also result in thrombocytopenia?

Case 3 pictures

Case 3 pictures 2

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• Legenda: Radiograph of lungs

Case 3 answers

• Question to ask - 'Have there been any injections given in that area?'
• Injection- septic myositis or local tissue reaction which could cause thrombocytopenia and epistaxis. In this case- no injections given, lack of moderate/ severe pain on palpation r/o septic cause of the swellings.
• DDx- guttural pouch mycosis (almost always unilateral clinical signs), thrombocytopenia, ethmoid haematoma
• Diagnostic test- ultrasound neck, leg, abdomen, and thorax
• Disease process- Neoplasia
• Diagnostic test- Needle aspirate of the mass. Revealed soft tissue sarcoma.
• Further diagnostics- determine cause of thrombocytopenia (excessive consumption, lack of production, increased destruction). Include meticulous microscopic examination of the platelets for reticulation (increased messenger RNA) or for large platelets- suggest increased release from marrow due to excessive loss of immune-mediated destruction of mature platelets. U/S or rectal examination - determine size of spleen (rectal - mucosal bleeding#0. Submission of blood to lab for flow cytometry - determine % of platelets bound with antibody = best test for immune-mediated thrombocytopenia. Bone marrow examination- determine if there is suppression of thrombocyte production.
• Lung radiography - Metastasis has occurred to the lungs, no obvious on radiography. Some circles of increased radiodensity- ? neoplasia. Lung radiographs- not sensitive for tumour metastasis in horse (size and loss of detail)
• Most common neoplasia - Haemangiosarcoma

Case 3 answers 2

• Follow up/ discussion
• Necropsy- Haemangiosarcoma of the neck (in muscle), metastasis to the regional lymph nodes, lungs and kidneys.
• Hind limb swelling- haemorrhage, no tumour in that location
• Two forms of haemangiosarcoma in horses- cutaneous/ locally invasive form (most often in the eye) may have a fair prognosis with proper treatment; disseminated form (often in muscle, lung, pleura, spleen, heart and kidney)- grave prognosis.
• Cutaneous/ ocular form - confused with haemangioma (local tumour).
• Haemangiosarcoma- common in middle aged horses.
• Systemic chemotherapy (doxorubicin) unlikely to be curative for the disseminated form.
• Treatment with local cisplatin and/ or surgical removal- curative for cutaneous or local forms

Case 3 picture answers

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• Legenda: Neck ultrasound- reveals a mass
• Legenda: Lung metastases identified on PME

Case 4

• 2month old Standardbred foal.
• 4 day history of laboured breathing, coughing, nasal discharge, mild depression.
• Foal- febrile, high temperatures (39.8oC).
• Foal treated - 3 days ceftiofur, gentamycin and ketofen w/o improvement.
• PE- foal bright and alert, harsh lung sounds bilaterally throughout the thorax, crackles and wheezes in the cranioventral thorax (using re-breathing bag). Thoracic ultrasound examination- bilateral, very small areas of cranioventral lung consolidation
• Primary differential diagnosis?
• Most common aetiologic causes for these signs?
• What diagnostic procedure should be performed next to gain further information
• What treatment should be recommended based on these results?

Case 4 answers

• Primary DDx- foal pneumonia
• Common aetiologies- Bacterial causes (Streptococcus zooepidemicus, Actinobacillus spp, Bordetella spp, Pastuerella spp, Rhodococcus spp). R. equi- less likely due to cranioventral location of the disease on ultrasound, but can't be r/o based on that distinction. Viral infection- predispose foal to bacterial pneumonia.
• Diagnostic procedure - CBC and fibrinogen- any above differentials expect a neutrophilic leukocytosis and hyperfibrinogenaemia are expected. Radiography, ultrasound - nearly as sensitive to detect pneumonia. Tracheal wash- performed and sample submitted for cytology, culture and sensitivity.
• Treatment recommendations- Cytologic evalation identified Pneumocystis carnii (yeast like fungal organism, uncommon, seen with R.equi and immunodeficiency syndromes). Actinobacillus spp was grown from bacterial culture. Foal treated with TMPS for bacterial/ fungal infections with an immune modulator (low CD4 T cells measures). Tested for IgG, IgM, IgA concentrations. Foal responded to treatment, clinically normal in 2 weeks.
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Case 5

• 9yo Thoroughbred. 2 month history of intermittent inappetence and weight loss. Previous tx- 2 weeks omeprazole and deworming (ivermectin/ praziquantel) w/o clinical response.
• Routine initial examinations- was unremarkable, low BCS (3/9) and 3/6 systolic murmur over left heart base, HR 48bpm.
• Gastroscopic examination- normal.
• Haematology and biochemistry- PCV 27%, plasma- white; Cl 88mEq/l, plasma protein 8.1g/dl, Cr 2.0mg/dl, anion gap 22mEq/l.
• Abdomen ultrasound - mottled appearance of spleen and left cranial abdomen (check pic on next page).
• Peritoneal fluid- colour (reddish), TP 5.3g/dl, RBCs 230,500 cells/ul, nucleated cell count 4,300/ul- 7% large round cells, 35% non-degenerate neutrophils, 32% small lymphocytes, 26% macrophages.
• What is the most unusual blood lab observation in this mature horse, how might it be associated with the clinical complaint?
• What additional lab tests should be performed based on these findings?
• What are the two major physiologic pathway abnormalities that might have caused the marked hyperlipaemia?
• With regard to the u/s findings what is the most likely diagnosis?
• In light of PME findings- what is the most likely mechanism for this horse's hyperlipaemia?

Case 5 pictures

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• Legenda: Red- peritoneal fluid; White - plasma
• Legenda: 5.2: U/s of abdome- spleen. 5.3: PME findings.

Case 5 answers

• Unusual blood observation- Low chloride concentration and high anion gap are interesting- related to increased lactact, sulfate or phosphate and the azotaemia. White colour of plasma indicates hyperlipaemia- very rare in horses. Hyperlipaemia- weight loss, intermittent inappetance and the primary disease.
• Additional lab tests - Measure lipids in plasma. Triglycerides - 1635mg/dl; cholesterol 368mg/dl; non-esterified free-fatty acids 0.54mEq/l
• Two pathways - Abnormal lipolysis and abnormal clearance of lipids (mostly triglycerides)
• Likely diagnosis - Neoplasia
• PME most likely mechanism - decreased clearance of very low-density lipoprotein likely due to lymphoma.
• Follow up/ discussion
• Neoplasm- confined to the spleen and surrounding area. B-cell lymphoma. Marked mineralisation of pulmonary artery, left atrium, renal tubules- hypercalcaemia and hyperphosphataemia.
• No microscopic evidence of hepatic lipidosis.
• Inhibition of lipoprotein lipase- reported in humans with lymphoma.
• Hyperlipaemia- severe to cause white coloured plasma = rare in horses (common in sick ponies/ miniature equines, occasionally Cushing's disease in horses - all these have hepatic lipidosis

Case 6

• 7yo Quarter Horse mare. Has chronic, foul-smelling, unilateral nasal discharge. Surgery performed under GA is right lateral recumbency.
• On recovery -mare was reluctant to bear weight on left forelimb, could extend leg when she walked, left triceps muscle felt very hard on palpation.
• Recovery of function in left forelimb- prolonged and painful- 7 days before mare would bear weight on the leg. As she began to bear weight- unusual sweating pattern occurred in left side of body - begin at withers and extended caudally.
• Most likely diagnosis for chronic, fetid-smelling, unilateral nasal discharge?
• How can it be confirmed?
• What treatment was probably provided?
• What was the likely cause of the complication in the left forelimb?
• What serum chemistry tests would help confirm this diagnosis?
• What would cause this unusual sweating pattern?

Case 6 pictures

Case 6 answers

• Most likely diagnosis - Septic sinusitis, tooth root abscess
• Confirm diagnosis - Radiography/ CT. CT revealed orosinus fistula and tooth root abscess of the left upper 3rd molar (tootl 211 in the Triadan system)
• Treatment provided - Flap sinusotomy. Affected tooth repelled, packing material placed in the tooth socket
• Likely cause for complication - a myopathy (not a neuropathy). Possible that there was some radial nerve paresis secondary to myopathy and swelling. Fracture of olecranon can also be considered.
• Serum chemistry tests - Measurement of muscle enzymes (CK/AST). Dark urine (myoglobin)- supports myopathy. Horse not tested for polysaccharide storage myopathy- would recommend
• Cause of unusual sweating pattern - damage to the sympathetic nerve pathways within the spinal cord at the most cranial site of the sweating (approx 3rd thoracic vertebra)
• Follow up/ discussion
• CK- elevates more quickly than AST. Blood sample 3hrs post recovery CK 2947 U/L, mildly elevated AST 387 U/L. Maximum values on day 3 post surgery: CK 44085, AST 1941. Day 15 post surgery: AST increased still 977, CK was normal 105- AST prolonged half life.
• 'Affected' limb was up during anaesthesia. Myopathies occur in either 'up' or 'down' limbs, peripheral neuropathies always in 'down' limbs.
• MIld hyperchloraemia and hyperglycaemia (due to stress) found on chemistry profile following surgery recovery. Cause- sympathetic dysfunction was not proven, injury to sympathetic nerve due to neuropathic inflammation/ pain was considered.
• Sweating- resolved in 3 days.

Case 7

• 21 yo Quarter horse gelding examined for pollakuria and dysuria, includes urine dribbling.
• Owners treated him with TMPS for 1 week- no change in clinical signs.
• Vital parameters - all normal, loud diastolic murmur was heard at base of the heart as stethoscope was passed cranially under left shoulder muscle. Horse was observed urinating- urine looked normal, free- catch sample was collected.
• Reasonable clinical work up in this case?
• Ultrasound image- interpretation
• What procedure could be performed to better visualised the urinary bladder?
• Most likely diagnosis based on information
• What are the two main bladder neoplasms in the horse
• Which one is most likely in this horse
• How could diagnosis be confirmed
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Case 7 answers

• Reasonable clinical work up - Urinalysis, abdominal palpation (rectal), ultrasound of the bladder. Urinalysis: USG 1.032, 3+ blood, 2+ protein, no leukocytes. No neoplastic cells on cytology. Rectal exam: large firm mass palpated as soon as hand entered rectum, mass extended 6-10cm beyond the brim of the pelvis and within the mass a smaller, possibly fluid-filled structure (? urinary bladder) could be felt. Soft tubular structure - palpated in the right- the ureter.
• Ultrasound image, interpretation- soft tissue mass can be seen within or next to a smaller fluid filled structure (likely ureter not the urethra)
• Procedure to better visualise bladder- Cystoscopic examination with sterilised 1 or 2 meter endoscope, allows improved visualisation if the lumen of the urinary bladder, ureteral orifices and urethra.
• Most likely diagnosis - Bladder neoplasia (based on age, clinical findings, urinalysis, ultrasound, cystoscopic examination
• Two main bladder neoplasms in the horse - Sqaumous cell carcinoma, Transitional cell carcinoma
• Which one is most likely - Transitional cell carcinoma due to pale homogeneous appearance of the mass, absence of gross haematuria. Sarcomas involving bladder muscle may also occur infrequently in younger horses.
• Confirm diagnosis- Biopsy taken during cystoscopic examination. Or tumour can be 'probed' with the scope and a urinalysis the collected for cytology (how carcinoma was diagnosed in this case). Necropsy examination confimed Transitional cell carcinoma with partial obstruction of the right ureter.

Case 7 answer- picture

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• Legenda: Cystological examination of the bladder- shows tumour

Case 8

• 10 month old Arabian Colt- rectal prolapse, poor body condition (BCS 2/9), not shed winter coat and chewing lice were present (Damalinia sp). Remainder of clinical examination, CBC, serum biochemistry were unremarkable.
• Colt dewormed (ivermectin/ praziquantel) after the prolapse was noted by referring vet 2 days earlier, faecal examination for parasites on admission was negative. 'Clump' of 1 x 2 cm flat parasites were seen attached to the mucosa adjacent to the prolapse.
• How should the rectal prolapse be treated?
• What is the most likely cause of the rectal prolapse in this colt?
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Case 8 answers

• Rectal prolapse treatment - Epidural anaesthesia due to to severe mucosal damage to the rectum
• Likely cause - Severe parasitic infection (3rd stage larvae of Gasterophilus intestinalis) which were passed
• Follow up/ discussion
• After placing epidural- prolapsed tissue was soaked and cleaned with hypertonic saline and the mucosa was coated with commercial haemorrhoid cream preparation.
• Prolapse manually reduced and a purse-string sutre was placed to prevent further prolapse.
• Suture loosened 4-6 times daily to allow defaecation, afterwards rectum was treated as described above and replaced.
• Colt given mineral oil by nasogastric tube and has mineral oil mixed into concentrate feed twice daily- soften manure.
• No prolapse occurred with defaecation after 4 days - fully recovered
• Condition causing prolonged tenesmus, irritation, injury and oedema of rectal mucosa- predispose to development of prolapse
• Occasionally seen in foaling mares, horses with diarrhoea and colitis
• Horses with diarrhoea- most common in those cases with NSAID toxicity,
• Gasterophilosis- thought to be cause in poorly managed colt, either G. intestinalis or G. nasalis may be associated with the condition.
• Prompt treatment of rectal prolapse and inciting cause- necessary to prevent progressive damage to the rectal mucosa. Severe injury to rectum occurred- submucosal resection may be required.

Case 9

• 12 yo Thoroughbred mare, 8hr old foal by her side. Presented for colic, trembling, abnormal sweating. Foal appeared to be normal. Assisted foaling- foal presented in normal anterior presentation and not a dystocia.
• Examination - mare restless, sweating, wanting to lie down (not violently colicky). Mildly hyperthermic (38.8oC), tachycardiac (80bpm), tachypnoeic (56bpm). MM- pale, slighty tacky, prolonged CRT (3 seconds). Rectal palpation- no intestinal distension, swelling palpated in right lateral abdomen just over brim of pelvis.
• Transabdominal ultrasound- increased free fluid of mixed echogenicity, some swirling movement to a maximum depth of 30cm.
• Rapid assessement test- normal PVC 42%, TS 6.0g/dl.
• What is the most likely diagnosis in this mare?
• What factors have been associated with an increased occurence of this condition?
• How can the blood volume of a horse be calculated, what percentage can be lost before a drop in blood pressure occurs?
• What treatments should be employed in a case like this, what should be avoided? What other clinica signs and bloodwork could help determine the mare's perfusion status
• Why are PCV and TS normal in this case?

Case 9 pictures

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• Legenda: 9.1: Mild colicking mare after foaling; 9.2: Ultrasound increased free fluid, mixed echogenicity with some swirling movement
• Legenda: What treatments need to be avoided- nursing foal.

Case 9 answers

• Most likely diagnosis - Middle uterine artery rupture. Uterine artery and its cranial and caudal branches are supported within the broad ligament (mesometrium), its branch of the external iliac artery- branch of aorta. Uterine artery - hypertrophied in pregnancy- rupture along it (often periparturiently) = rapid haemorrhage. Blood clot- forms in broad ligament, blood still leaks into abdomen. Initial blood clot is dislodged/ ruptures- massive, fatal intra-abdominal haemorrhage often ensues.
• Factors associated with this condition- Rupture of uterine artery. More common in multiparous, older mares, assisted births (foal pulled manually), dystocia- source of trauma. Normally right side ruptures- increased tension on broad ligament as gravid uterus displaced to the left by the caecum. Association between low copper levels, increased vessel fragility- predispose to rupture.
• Calculate blood volume of the horse, what percentage can be lost before drop in blood pressure- Blood volume = 8-10% of body weight - blood volume is 40-50L for 500kg mare. Horse can lose 20-30% of intravascular blood volume (8-12L in this 500kg mare) w/o drop in BP due to increased cardiac output and vasopressor, endocrine, renal compensatory mechanisms.
• Treatments employed/ avoided. Other clinical signs/ bloodwork - Rupture can lead to rapid death no matter what treatment methods are used- survival is possible esp when majority of haemorrhage is in broad ligament. Keep mare quiet and calm- avoid dislodging clot fomation. Hypertensive horses- agitated easily so quiet environment/ light sedation beneficial. Blood loss is great ( HR> 100m mm-white, weak, ataxic, increased blood lactate levels)- any sedation = collapse. Maintain permissive hypotension with controlled volume of isotonic fluids +/- blood transfusion (systolic BP 70-90 mmHg) to minimise ongoing haemorrhage and risk of clot disruption. Abdominal bleeding is stable/ no respiratory distress- don't drain abdomen because increased abdominal pressure can reduce ongoing bleeding and 2/3rd intra-abdominal erythrocytes will autotransfuse and components will be utilised. Aminocaproic acid (30mg/kg IV in 1L 0.9% NaCl)- antifibrinolytic, maintain clot stability. Whole blood transfusion PCV < 20% in 12hrs, <12% in 24-48hrs, lactate is high or PvO2/SvO2 are low.
• PCV/TS are normal - Acute haemorrhage all blood components lost equally, unless crystalloid therapy given IV, need 4-8hrs for aldosterone/ vasopressin to have dilutional effect on PCV and plasma protein via renal absorption of electrolytes/ fluids. Horses- acute haemorrhage - die from lack of circulating RBCs in face of normal PCV/ plasma protein concentration.

Case 10

• 26yo donkey jenny. Presented for further diagnosis of shifting weight in hindlimbs, reluctance to move, placing hindlimbs abnormally far under the body, progressive anorexia (2weeks duration). Donkey treated with ceftiofur and flunixin meglumine for previous 10d, no improvement. Been on same farm for last 12yrs, kept with 3 other donkeys and 8 horses- all healthy. No health problems noted previously, excellent routine vaccination, deworming, dental care.
• Presentation- good to fat body condition, depressed. Mildly hypothermic (36.4oC), tachycardic (96bpm), normal respiratory rate (24bpm). MM- dark pink, tack , CRT 3.5seconds. Absent GI sounds, rectal revealed dry manure and a pelvic flexure impaction. Increased PCV 53%, TS 86g/l. Serum in microhaematocrit tube was opaque, whitish discolouration.
• What does abnormal serum colour mean, what biochemical test would provide more information concerning this abnormality? Is this condition important, what therapy should be used to treat it?
• Donkey - dehydrated, possibly for a prolonged period since illness has been progressing over 2 weeks. What organ system is of immediate concern with respect to secondary effect, how should this be investigated?
• Donkey stopped shifting weight in the hindlimbs after abaxial sesamoid local nerve blocks performed in both hindlimbs. What condition is most likely responsive for this clinical sign of weight-shifting, what could be done to further assess this and make donkey comfortable
• 5 days hospitalisation and aggressive, intensive medical therapy- donkey clinically improved: vital signs normalised, pelvic flexure impaction resolved, haematologic parameters returned to WNL, laminitis pain controlled. Donkey still anorexic, quiet and depressed
• 4. What could be the cause of this, how can it be remedied>

Case 10 pictures

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• Legenda: Sick, depressed anorexic donkey
• Legenda: Serum - opaque and whitish appearance

Case 10 answers

• Abnormal serum colour, condition- Hyperlipaemia- further assessed by measuring serum triglyceride levels (<66mg/dl in normal donkeys). Hyperlipaemia - secondary to negative energy balance and mobilisation and ultilisation of fat for energy. Common in donkeys with illness, stress or any situation where there is inadequate feed intake. Jennies and overweight donkeys- at risk of developing hyperlipidaemia and hyperlipeamia. Hyperlipaemia- very serious condition; clinical signs- anorexia, depression, icterus, colic, weakness, incoordination and death (untreated); tx- force feed mix of glucose, electrolytes and sodium bicarbonate and. or proprietary 'critical care' meals. IVFT with B vitamins and/ or partial parenteral nutrition- also administer. Insulin therapy, broad-spectrum abx and flunixin meglumine may be needed (severity of disease).
• Donkey dehydrated, system affected- Assess renal function in face of marked (possibly chronic) dehydration. Further diagnostics- serum biochemistry (creatinine, BUN, electrolytes), urinalysis, renal ultrasonography
• Stopped shifting hindlimbs after block, condition - Positive response to abaxial nerve block, indicated weight-shifting due to foot pain (likely laminitis) Radiographs can confirm this. Response to hoof testers- unreliable in donkeys. Laminitis-common in overweight donkeys (lameness, abnormal stance, reluctance to move)- more subtle than in horses due to stoic nature. Elderly donkeys- chronic laminitis changes, suffer acute bouts unnoticed- same for colic (donkey has impaction- no signs of abdominal pain). This case- suffered acute laminitis --> reduced feed/ water intake (pain/ reluctance to move)--> secondary hyperlipidaemia--> impaction due to low water intake. Tx - deep bedding, NSAIDS (analgesia) , address underlying cause). NSAIDs- well tolerated in donkeys, suffer GI/ renal side effects less than horses.
• Whats the cause and how can it be remedied- Donkeys form strong bonds with each other/ other animals. Remove donkey from its home/ herd mates --> anorexia, depression in absence of clinical disease. This case- companion horse was brought in to the hospital for company and donkey immediately became brighter and began to eat.

Case 10 picture answer

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• Legenda: Donkey with laminitis

Case 11

• 2yo Arabian gelding from New York presented in Summer after 4 days of intermittent fever (40.3oC). Horse's temp taken BID, single dose of phenylbutazone (2.2mg/kg PO) had been given 5 times (when temp > 39.4). 25 other horses housed at training facility, none reported to be sick. Horse- fit body condition, performing well in training for 4 months. Horse last worked 24hrs prior to development of fever.
• Presentation: very quiet, mm- hyperaemic, CRT 2.5 seconds. GI sounds- hypermotile in all 4 quadrants. Rectal- normal manure, no abnormalities. Horse- normothermic (38.1), tachycardic (60), tachypnoeic (40). Large plaque of non-painful pitting oedema on ventral abdomen and thorax. CBC abnormalities- increased PCV (49%), leukopenia (41,000 cells/ul), profound neutropenia (100 cells/ul), immature band neutrophils (500 cells/ul), moderate toxic changes and thrombocytopenia (64,000 cells/ul). Biochemistry abnormalities- hyponatraemia (124mEq/l), hypochloraemia (92mEq/l), hypoproteinaemia (5.2g/dl) due to hypoabluminaemia (1.9g/dl), decreased colloid oncotic pressure (9.8mmHg), decreased bicarbonate (20mEq/l). Urinalysis, BUN and creatinine were normal.
• Presented to ERH- where should patient be housed and why?
• Primary differential diagnosis in this horse - based on hx, location, time of the year, clinical signs, haematology
• Treatment choice for the disease
• Important secondary complications that can occur

Case 11 picture

Case 11 answers

• Where should horse be housed- Housed in isolation due to history of fever and leukopenia with neutropenia evident on CBC.
• Primary differential- Potomac horse fever (PHF): aetiologic agent is Neoricjettsia risticii- transmitted by accidental ingestion of the metacercaria stage of trematodes (snails) present in larval and adult aquatic insects (caddisflies, mayflies). Not uncommon to see normal manure in early stages of disease/ if patient is dehydrated- diarrhoea occurs once rehydrated, some never develop diarrhoea. Other differentials- right dorsal colitis secondary to PBZ admin; salmonella; Clostridium difficile; infiltrative bowel disease- lymphosarcoma or granulomatous inflammatory bowel disease; cyathostomosis. These differentials are considered due to protein most likely lost through GI tract (unlikely to be renal - normal urinalysis, unlikely to be liver- no icterus/ no elevation of liver enzymes/ also healthy and training well week before). Hypermotile gut sounds- evidence of GI disease. PHF most likely due to location (New York), time of year (summer), evidence of GI disease.
• Treatment of choice- Oxytetracycline (6.6mg/kg IV q12hr) for 5 days, supportive care. Treatment response- good.
• Secondary complications - Laminitis develops in 15-25% of cases, often reason for eventual euthansia.

Case 12 case

• 9yo Arabian mare- barrel racer. 12 month history of reduced exercise tolerance. Four months prior- fever, lameness, ventral oedema, heart murmur. Most recently- exercise intolerance obvious nostril flare, RR 70 when walking. Severely depressed, ataxic in all 4 limbs, bilateral jugular vein distension and pulsation, HR 70 (>90 after walking), 4/6 systolic heart murmur heard over left pulmonic valve area. Lungs ausculation- WNL. Echo performed- right atrium and ventricle appeared enlarged, left ventricle and atrium appeared smaller.
• CBC- for evidence of infectious/ inflammatory process, severe clinical signs correlated with fever. Lab findings: leukocytosis 11.2 x 10^9/l; PMNs 7.8x10^9/l; fibrinogen 3g/l. Arterial blood gas: pH 7.42; PCO2 39.7mmHg; PaO2 100mmHg; HCO3 25.6mEq/l, O2 saturation 98%; lactate 1.88mmol/l. cTnI 0.00; AST 675 IU/l; GGT 276 IU/l; SDH 14 IU/l
• Interpret echo findings
• What do the CBC abnormalities suggest?
• Which of the following is the most likely diagnosis: Cor pulmonale- pulmonic vavlular stenosis; cor pulmonale - diffuse pulmonary parenchymal disease; cor pulmonale- obstruction of the pulmonary artery?

Case 12 pictures

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• Legenda: 12.2: long axis view from the right chest- RV/A enlarged, LV/A smaller than normal. 12.3: velocity of flow over the tricuspid valve
• Legenda: 12.4/5: size comparison between aorta and pulmonary artery

Case 12 answer

• Echo findings - Clinical and echo findings supportive of right heart dilatation and tricuspid insufficiency. Small left ventricle/ atrium - volume contraction. High velocity flow over tricuspid valve- obstruction of pulmonary artery. If tricuspid insufficiency is the only problem (valvular degeneration)- no high velocity flow, usually only moderate pressure differences between RV/A. This case- right ventricular hypertrophy- related to pulmonary artery obstruction causing marked difference in pressures between the two chambers. The pulmonary artery- larger than the aorta- dilatation of the pulmonary artery. No obstruction noted at pulmonic valve.
• CBC abnormalities- Normal arterial oxygenation, modest elevation in lactate- decreased perfusion. Elevated liver enzymes and ventral abdominal oedema- due to right sided failure/ congestion
• Most likely diagnosis- Cor pulmonale -obstruction of pulmonary artery.
• Follow up/ discussion
• Necropsy- large firm mass found on pulmonary artery (plaque in the centre of opened pulmonary of picture on next slide). Pulmonary artery and aorta- 16cm diameter; aorta should be larger than pulmonary artery. RV wall thickness- 2cm; LV wall was 3cm.
• Mass- fibrous connective tissue, degenerate neutrophils, large number of fungal organisms- Aspergillus spp.

Case 12 picture answer

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• Legenda: Plaque visible in centre of the pulmonary artery. Identified as aspergillus.

Case 13

• 2 day old Thoroughbred colt- milk observed at both nostrils after nursing. Foal - delivered without complications, umbilicus dipped with hibiscrub at 15 and 30 minutes after birth, enema given 1hr after birth. Foal stood normally, nursed within 1hr. Vitamin E and selenium IM injection on first day of life. Clinical exam on day 2 - normal except milk observed at nostrils.
• What are the R/Os for milk refluxing into the nasopharynx and nostrils in a newborn foal?
• What diagnostic procedures should be performed to investigate milk refluxing from the nostrils?
• What abnormality is seen in endoscopic image of the larynx (13.2)- how might it explain clinical signs and future use of the foal?
• What routine test should be performed to make sure foal had adequate absorption of maternal antibodies? How quickly after nursing can the test be accurately performed?
• 

Case 13 answers

• Differentials to R/O- Cleft palate, white muscle disease (selenium deficiency), persistent epligottic frenulum, hypoxic ischaemic encephalopathy, megaoesophagus, vascular ring anomalies, pharyngitis/stomatitis/oesophagitis, oesophageal choke, fourth branchial arch defect, weak foals (e.g. systemic illness, electrolyte abnormalities, hypoglycaemia)
• Diagnostic procedures - Examine oral cavity for defect in the hard palate (was normal). Endoscopy of upper respiratory tract- abnormalities in soft palate, distal pharynx, larynx
• Abnormalities in endoscopic image - Foal (unsedated) has rostral displacement of the caudal pillar of the soft palate over the right arytenoid cartilage, less abduction of the right arytenoid cartilage compared to the left one. External palpation of larynx - gap between thyroid and cricoid cartilages. Defect not felt on the left. Suggests right sided fourth branchial arch defect- more common than let sided defect. Loss of muscle fibres at proximal oesophagus- involved in defect- involuntary aerophagia (chronic colic in some horses), proximal oesophageal dilation. This case- foal believed to be swallowing normally, when head is lowered after nursing- reflux of residual milk from oesophagus. Affected foals unlikely to be effective racehorses- instability of larynx.
• Routine test to check maternal anitbodies - Foal checked for adequate IgG between 14 and 24hrs after first nursing. On-site ELISA (Snap Foal IgG Test, Idexx)- determine adequate passive transfer of colostral antibodies.

Case 14

• 19yr old Quarter Horse - acute onset of paresis of the mandible and lower lip. Horse last seen normal 12hrs prior to presentation when turned out to pasture for the night. Owner first noticed abnormality when they brought the gelding in that morning. Horse seemed unable to eat/ drink- attempting to do so.
• Examination- quiet, responsive, mm-pink, CRT 1.5seconds. Normothermic, mildly tachycardic (48), normal RR (20).
• Neurologic examination - symmetric lower lip droop with decreased to absent sensation of the lower lip and gums adjacent to both first mandibular incisors. Horse able to weakly appose upper and lower incisor teeth. Tongue tone - normal. No obvious swelling or muscle atropy evident on head/ neck. All other CN testing- WNL. Remainder of exam- normal.
• Offered soft bran mash- able to slowly prehend, masticate and swallow.
• Neuroanatomic lesion in this horse?
• How might it had occurred?
• What important neurologic disease can produce these clinical signs as part of its constellation of possible symptoms?

Case 14 pictures

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• Legenda: Acute paresis of mandible
• Legenda: Acute paresis of lower lip

Case 14 answers

• Neuroanatomic location - Clinical signs reflect bilateral lesion to the mental branches of the mandibular branch of trigeminal nerve (CN5). Mental branch - sensory to lower lip, muzzle, gums. Peripherally mental nerve branch carries motor fibres from the buccal branch of the facial nerve (CN7)- accounts for lower lip droop. Weak closure of lower jaw- more proximal injury to the mandibular nerve before mental nerve branches off.
• How did lesion occur- Focal and bilateral lesions= local insult to nerve branches. Mental nerve emerges from mental foramen in the mandible- superficial, vulnerable to trauma. e.g. bilateral lesion- horse had muzzle trapped in narrow space then panicked and pulled back with force/ prolonged period. Injury from a bit might be the cause of signs- no suspicion in this case. Idiopathic trigeminal neuropathy- common in dogs, rare in horses.
• Important neurological disease - Dropped jaw and drooping lower lip can be part of the clinical signs of rabies - variety of neurologic presentationss, always a progressive fatal disease.
• Discussion/ follow up
• This case- cause not determined.
• Tx- dexamethasone (0.1mg/kg IV q24hr) for 2 days, thiamine (10mg/kg IV q24h) for 5 days, vitamin E (20 IU/kg PO q24h) for 14days
• Gelding improved gradually- 3 weeks after initial onset- assessed as normal by the owners
• Dogs - idiopathic trigeminal neuropathy- mean time to recovery w/o tx = 22days

Case 15

• 2 month old Warmblood foal - diarrhoea of 3 days duration, mild fever, swollen hocks w/o lameness. No prior medical tx and 20 other foals on farm- unaffected.
• Clinical exam - bright and alert foal, normal HR/RR, normal thoracic ausculation, fever of 39.4. Diarrhoea- frequent, low volume. Hocks swollen, no lameness observed at walk. Skin -normal. Not dehydrated.
• CBC- WBC 7.5x10^9/l with mature neutophils 5.3x10^9/l), PVC 24%, fibrinogen 5g/l, TP 5g/l.
• Serum biochemistry- slight hyponatraemia 130mEq/l, hypokalaemia 2.6mEq/l.
• What are the differential diagnoses for diarrhoea/ fever in 2 month old foal?
• Diagnostics to be performed
• Why might hocks be swollen with little/ no lameness?
• Foal treated with clarithromycin, metronidazole, ripampin and omeprazole PO, IVFT- diarrhoea resolved within 6 days. Despite of good nursing and bandaging swollen hocks - foal developed unusual perineal dermatitis.
• 4. What could be the cause of the dermatitis?

Case 15 pictures

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• Legenda: Sick foal - diarrhoea and swollen hocks
• Legenda: Diarrhoea resolved - developed perineal dermatitis

Case 15 answers

• Differential diagnoses - Rotavirus, Clostridium perfringens A, Clostridium difficule, Salmonella, Rhodococcus equi, acute strongyle infection, cryptosporidosis. Unusual to have isolated case of salmonella or rotavirus. Infection with C. perfringen A - difficult to prove since organism (even enterotoxin) can be found in manure of normal foals. Cryptosporidosis and acute strongyle infection- not common.
• Diagnostics - Aerobic faecal culture- look for Salmonella soo, R. equi; ELISA/ electron microscopy on faeces - rotavirus; toxin testing - C. difficile and C. perfringens (foals- toxigenic C. difficile may cause diarrhoea w/o hx of abx; faecal smear/ flotation - cryptosporidium. Faecal gram stains- rarely clinically useful in foals.
• Swollen hocks with little/ no lameness - Indicate immune-mediated synovitis- frequently found with R. equi infections
• Cause of dermatitis - multifocal, raised, red nodules- not characteristic of contact dermatitis due to diarrhoea (dermatitis- more uniform throughout diseased area). Nodules are raised- infectious agent. Biopsy revealed granulomatous dermatitis- PCR positive for R. equi.
• This case- large amount of R. equi in the faeces and infected perineal skin.

Case 16

• 7month old Thoroughbred colt treated with IV fluids on farm- anorexia and suspected gastric ulcers. Foal developed septic thrombophelbitis of jugular vein, treated with chlorophenicol PO for 3 days w/o improvement, referred for evaluation.
• Important lab findings -axotaemia, hyponatraemia, hypochloraemia, anion gap with an l-lactate 2.8mmol/l. USG 1.14. Azotaemia resolved over 72hrs with fluid therapy. Within 36hrs of hospital admission spiked fever (39.4), developed lameness in both forelimbs, swelling of R carpus and L fetlock.
• Most likely reason for lameness?
• Diagnostic procedures that could be performed to determine aetiologic cause?
• What are the treatment options?
• What would be the benefits of therapeutic drug monitoring in this case?
• Foal seemed to improve, but fell when trying to stand immediately following regional limb perfusion tx, acutely non-weight bearing in R hindlimb. Ultrasounds of medial aspect of the semimembranosus muscle
• 5. What are the differentials and likely cause for this rapid swelling and new lameness?

Case 16 pictures

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• Legenda: Sick foal- anorexic, swollen carpus/ fetlock, azotaemic
• Legenda: Ultrasound of semimembranosus muscle, large swelling

Case 16 answers

• Most likely reason for lameness- Septic arthritis secondary to septic thrombophlebitis and bacteraemia
• Diagnostic procedures - Aspirate joint fluid from the carpus, evaluate for viscosity (visual), lab to determine cell count, TP, cytologic evaluation, bacterial culture. Aspirate jugular vein abscess following ultrasound examination. Blood cultures could be performed - discontinue abx for 24hrs. Uncommon to obtain positive cultures from joint-fluid in foals with bacteremic-induced septic arthritis because bacteria found in synovial membrane. This foal- thrombosed jugular vein was aspirated, grew Staphylococcus spp. (not MRSA) resistant to most abx not enrofloxacin, gentamicin and amikacin.
• Treatment options - Abx (bactericidal) are indicated. Enrofloxacin not chosen due to foal's age. Gentamicin can be cautiously given (azotaemia- that has resolved). Potassium penicillin IV (gram + coverage), NSAIDs IV. Amikacin- regional IV perfusion to affected limbs SID 3d, Joint lavaged once - isotonic sodium bicarbonate, amikacin. Omeprazole- PO. IV fluids- catheter in lateral thoracic vein.
• Benefits of therapeutic drug monitoring - Verify that gentamicin peak concentration (30-60 minutes after administration) was 10x MIC of Staphylococcus grown would be important when treating life-threatening infection. Foal recovering from AKI- trough level was <1.0ug/ml
• Differentials - Fracture (pelvis/ femur), rupture of tendinous insertion in caudal thigh. This case- no fracture identified, foal improved following day. Rupture of gastrocnemius insertion- incomplete as reciprocal mechanism between hock- stifle intact. More likely- rupture of gracilis muscle- good prognosis for recovery, fibrotic myopathy- occur later in life.

Case 17- Colic/ depression in foal

• Signalment - 48hr old colt. Colic, lethargy, disinterest in nursing.
• Presentation- depressed, normothermic, tachycardic, tachypnoeic, mm- pink, injected, slightly tacky. CRT 2.5 seconds. Moderate abdominal distension. Abdominal U/S -free abdominal fluid. Biochemistry - hyponatraemia, hyperkalaemia, azotaemia. Also been straining.
• Most common causes of colic/depression in foals
• Meconium impaction - most common (< 3days). Resolve with enemas, oral laxatives- most breeders administer enema to foals to prevent this
• Enterocolitis- begins with depression, pyrexic. Causes - salmonella, Clostridium perfringens, secondary to generalised septicaemia.
• Uroperitoneum - more common in colts. Ruptured bladder, also be ureters and urethras.
• Most likely aetiology
• Signalment, clinical signs (straining, abdominal distension, mild colic, depression), U/S findings (free fluid), and lab work abnormalities - uroperitoneum.
• Diagnostic test
• Abdominocentesis- fluid clear to yellow, creatinine double or more than serum level (fluid is urine). U/S examination- identify ruptures
• ECG abnormalities - hyperkalaemia
• Spiked/ tented T waves, blunted/ absent P waves, prolonged QRS/ PR, shortened QT. IF severe - fatal bradycardia.
• Initial treatments
• Ruptured bladder - surgery needed. Need to stabilise medically beforehand0 IV fluids (NaCL) dextrose (IV), - lower potassium (move intracellularly). IV calcium borogluconates - ECG abnormalities due to hyperkalaemia. Peritoneal drainage - lower potassium/ creatinine, improve RR, HR prior to sx. Prophylactic abx- needing intraperitoneal drain placed, bladder may be septic. Check IgG levels -passive transfer; inadequate need plasma transfusion.

Case 18 swelling on neck- vaccine reaction

• Signalment- 3yo Thoroughbred- swelling on L side of neck. Duration- 1 week, after vaccination with modified live intra-nasal strangles and IM west nile virus in left neck. Swelling- same location as vaccine. Increased in size over 5 days, horse- febrile (39.7)
• Likely cause of swelling
• Streptococcus equi equi abscess caused by vaccination. Two possibilities - modified live intra nasal vaccine there was contamination of the neck or West nile virus vaccine needle with S.equi; intranasal vaccine - bacteraemia. IM vaccine - hyperaemia at the site, S.equi colonised and formed an abscess. Don't give additional vaccines with modified live intra-nasal vaccine.
• Best treatment
• Abscess - drain and culture for abx sensitivity of organism. 1-2weeks abx course- based on results.
• Isolation?
• Yes- while abscess is draining. Disinfect all in contact areas. Rarely transmit the bacteria - need to be cautious with other horses.
• Organism survival in environment
• <24hrs in sunlight, indoor environment - several days.
• Horse- chronic shedder?
• Culture/ PCR of guttural pouch wash (endoscopy) detect carriers. Single nasopharyngeal flush- detects fewer carriers, nasal swab for culture/PCR- negative in many carriers.
• Confirm organism cultured was from the vaccine
• Bacterial colonies of vaccine strain - more mucoid than natural strain. PCR testing - confirm abscess from vaccine strain. Positive PCR- doesn't mean live organisms are present.

Case 19 - Ionophore Toxicity

• Signalment - 4yo Thoroughbred. 3 day hx mild ataxia, severe progressive weakness --> recumbency. Bright and alert, normothermic. HR 54. Neurologic exam - decreased muscle tone of limbs, normal tail tone, eyelid tone and ability to eat. Increased muscle enzymes, no muscle atropy. Mild hyponatraemia and hypochloraemia. TX- IVFT for electrolyte imbalances for 48hrs, no clinical improvement.
• Botulism- tentative diagnosis, some clinical findings don't match.
• Horses with botulism- diffuse neuromuscular weakness including tail tone, eyelid tone and dysphagia. This horse has normal eyelid tone, tail tone and ability to eat.
• Other differentials for skeletal muscle weakness
• Equine motor neuron disease, magnesium toxicity, lead poisoning, organophosphate toxicity, hypocalcaemia, hypokalaemia, ionophore toxicity, tick paralysis, primary myopathies
• Follow up/discussion
• Further history- horse fed lasalocid (calf coccidiostat) by accident for 6 days. Horse was euthanised, no ionophore testing was performed.
• Post mortem histopathology - axonal swelling and corresponding nerve/ muscle degeneration throughout cervical to sacral area. No evidence of cardiac necrosis - cardiac troponin I testing no available at the time. Tentative diagnosis - ionophore toxicity with peripheral neuropathy and myopathy.
• Ionophore toxicity- common cause is monensin- causes acute colic, sometimes diarrhoea immediately followed by signs of cardiac dysfunction. Ataxia and skeletal myopathy--> recumbency in some cases.
• Lasolocid and salinomycin - cause skeletal and cardiac myopathy and neuropathy in horses
• Salinomycin- more toxic than monensin (mg/kg basis)- toxicity is rare as less commonly used in livestock feeds.
• Lasolocid- less toxic than monensin (mg/kg basis)
• Ionophore toxicity prognosis - guarded to poor, poor if cardiac involvement.

Case 20- EHV 1, foal

• Signalment - 36hr Standardbred colt- failure to actively nurse during first 24hrs. Clinical examination - unremarkable, mild weakness, lack of affinity for the mare. Normothermic, HR 140, RR 40, auscultation was abnormal. Foal given plasma transfusion (low IgG), started on Abx (ceftiofur 5mg/kg IV), recieved intranasal oxygen.
• Abnormal CBC results- WBCs 1x10^9/l, neutrophils 0.79x10^9/l, bands 0.2x10^9/l, lymphocytes 0.1x10^9/l, platelets 82x10^9/l, moderate toxic changes in neutrophils. Biochemistry- bilirubin was high 120umol/l, normal SDH 4IU/l, low AST 185 IU/l, normal GGT 20 IU/l)
• Despite abx, transfusion, IVFT and flunixin meglumine- foal developed progressive respiratory distress over next 20hr, died suddenly. Necropsy examination - striking lesions in the lungs and serosal surface of small intestine. Enteric mucosa appeared normal.
• Interpretation of foal
• Failure of passive transfer, tachycardic, lab changes suggest sepsis (is normothermic). Low WBC count- gram negative sepsis or viral infection
• Placenta 12% foals BW- interpretation.
• Normal equine placenta should be no more 11% foals BW. Increases - oedema from infectious causes (placentitis), toxic insults.
• Foal rapidly deteriorated- interpretation, gross pathology findings
• Diffuse consolidated appearance of the lungs in a foal that has normal RR/effort for first 24-36hrs = acute interstitial pneumonia. Multifocal haemorrhagic lesions in small intestine/ normal mucosa- vasculitis.
• Most likely differentials
• Interstitial pneumonia - Equine herpes virus 1, equine viral arteritis, possible adenovirus.

Case 20 part 2 EHV 1

• Discussion/ follow up
• Foal positive for EHV-1 in liver, lung, lymphoid follicles of small intestine.
• Analysis of virus via PCR- 'neuropathic' strain of EHV-1. 70% of equine herpes myelopathy cases due to mutation of neuropathic strain; 25% of EHV-1 abortions are from this strain.
• Neonatal death- rare in foals. Rare for neonatal EHV-1 to transmit infection and neurologic disease to adult horse. Contact with placenta (virus laden)- cause of adult horse infection.
• Infected adult- recieved steriods for another problem - predisposed to high EHV- 1 viraemia and subsequent neurologic signs.
• This foal - didn't transmit virus to other adult horses, did have contact with several horses during his viraemia.
• Adult horse- gradual improvement of neurologic signs.
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• Legenda: Post mortem of foal- multifocal haemorrhagic lesions in small intestine. Consolidation of the lungs.

Case 21-Vasculitis

• Signalment- 13yo Morgan gelding. Fever and pruritus. 6 days earlier- acutely developed pruritic hives on the neck, shoulders and abdomen while being ridden. Appeared to recover w/o tx- 2 days later developed swollen legs and sheath. Generalised oedema, pruritus and generalised dandruff.
• PE- temperature 44oC, tachycardia HR 54. Legs and ventral abdomen - pitting and painful oedema. Evidence of thickened skin, hair loss over face, neck, dorsum. No petechiation on mm, no recent hx of drug administration/ infectious disease exposure.
• Generalised disease type
• Vasculitis
• DDx - Immune mediated inflammatory disease of blood vessels, associated with bacteria, drugs, viruses, other environmental or chemical factors (sun exposure). Purpura haemorrhagica- most common disorders of vasculitis in the horse.
• Diagnostic tests - Skin biopsy , revealed leukocytoclastic vasculitis, oedema, haemorrhage, hyperkeratosis. Other tests- endoscopy of guttural pouch, PCR- Streptococcus equi equi, serology - EVA, testing (serology/ PCR) -anaplasmosis.
• Treatments- Dexamethasone (20mg IV) SID until clinical response observed. Taper dose over 10d period. Due to crusting of the skin, systemic penicillin and medicated shampoo (ketaconazole and chlorhexidine) can also be given.
• Primary concern with drug in this case - Corticosteriod induced laminitis. Short term tx, moderate doses- rarely cause laminitis unless horse predisposed to due to endocrine disorder (Cushings, insulin dysfunction/ metabolic syndrome). Morgan horses- high incidence of equine metabolic syndrome (phenotype- abnormal fat deposits).

Case 21 - Vasculitis pictuces

Case 21 Vasculitis discussion

• Cutaneous vasculitis- common problem, inciting antigen/antibody not confirmed in >50% cases.
• Painful oedema of limbs and other areas of the body, scales and crust- most common clinical findings.
• Purpura haemorrhagica- petechiation of mm's and occasional fever- diagnosis based on clinical findings (skin biopsies not highly sensitive)
• Treatment - immunosuppressive therapy with corticosteroids or azathioprine, address inciting infection (S. equi)
• Pentoxifylline (inhibits cytokines)- also used to treat vasculitis, given to effect to control signs.
• Dexamethasone dose - variable, give to effect to control signs. High doses (80mg/day) have been used, 30-40mg/day is standard starting dose. More effective than oral prednisolone.
• Horse- responded to treatment, signs recurred when prednisolone (400mg PO daily) was substituted for dexamethasone. Dexamethasone restarted- 20mg IV SID, taper dose over another 10 days- effective in resolving disease.
• Tx for vasculitis and pemphigus foliaceus- very similar; horses with vasculitis completely recover, pemphigus- controlled not cured.

Case 22 - Neonatal isoimmune thrombocytopenia

• Signalment- 3day old Warmblood colt. Acute onset salivation, 'matted' eyes, difficulty nursing, multifocal dermatitis over head/ neck region.
• Uncomplicated foaling, adequate colostrum, umbilicus dipped with dilute hibiscrub TID, recieved injection of vitamin E and selenium (1 ml) in hindlimb. Foal- normal for 2 days.
• Exam on day 3- normothermic, normal HR/RR. Other abnormalities- ecchymotic haemorrhages and erosions in the mouth. Owners commented foal must have eaten something toxic.
• Diagnosis for foal based on clinical signs - Neonatal isoimmune thromboctyopenia. Historically- immune reaction to naval dips were implicated in pathogenesis of this disease- likely erroneous
• Recommended lab test - CBC. Platelets 3x10^9/l, neutrophils 2.8x10^9/l. Thrombocytopenia- most dramatic abnormality in this disorder, most foals also have neutropenia.
• Treatment and complications - Confine foal to stall/ small paddock to limit exercise, possibility of haemarthrosis. Administer corticosteroids (rec tx)- rebound in platelet count. 0.1mg/kg dexamethasone PO/IM/IV with 1 week tapering dose. Injections - haematoma formation, small gauge needle should be used, vein tightly compressed after blood collection/ injection. Repeat platelet count- aderse effects of maternal antibodies on platelets can last 3 or more weeks. This foal - haematoma after IM injection, resolved w/o complication, platelet count quickly rebounded. Foal also treated with sucralfate, omeprazole and TMPS.
• Recommendations to the owner- Colostrum from mare risks same condition in future foals. Unlike neonatal isoerythrolysis- no proven test to determine risk to foals
• What does mean platelet volume (MPV) indicate - Measurement of mean platelet size, increased value indicates bone marrow is responding to thrombocytopenia- marrow releases immature platelets (larger than normal- increased RNA). Increased MPV- thrombocytopenia is due to excessive comsumption/ destruction, not lack of production.

Case 23- Guttural pouch diseases

• Signalment- 10yo Thoroughbred gelding, pleasure horse. 3wk hx of cough and bilateral mucopurulent nasal discharge with ssome food material at nares. Coughing pronounced when horse is eating. Some weight loss, horse - underweight. 10d course of TMPS PO- no noticeable improvement.
• Clinical exam- horse bright and alert, vital signs -normal. No gait abnormalities/ abnormal CNs. Chest auscultation- few crackles/ wheezes in right ventral area. Thoracic u/s performed.
• Endoscopy of oropharynx- food material in trachea, soft palate easily displaced. Lesion observed within medial compartment of right guttural pouch.
• Major concerns to clinical conditions affecting horse - Dysphagia- due to neurologic disease, possibly aspiration pneumonia.
• Thoracic ultrasound- Cranioventral pulmonary consolidation- due to aspiration pneumonia. Typical for aspiration pneumonia more severe on the right side of the lungs (seen in this case).
• Organisms associated with this pneumonia - Streptococcus equi zooepidemicus, Actinobacillus spp, Enterobacter spp, E.coli, S.aureus, numerous anaerobic organisms.
• Most likely diagnosis- Fungal lesion- damaged the medial pharyngeal branch of the vagus nerve, caused dysphagia--> subsequent aspiration pneumonia.
• Treatment options for guttural pouch lesion - Topical antifungal tx preferred. Local tx options- nystatin powder, natamycin, micoconazole, clotrimazole, 2% enilconazole solutions. Irritating products (iodine and chlorhexidine)- never place in guttural pouch due to severe and irreversible paralysis. Additional therapeutic options - itraconazole PO, sodium iodide IV

Case 23- guttural pouch disease pictures

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• Legenda: 23.1: U/S of thorax- consolidation due to aspiration pneumonia. 23.2: Fungal lesion in guttural pouch.
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• Legenda: 23.4: Anti-fungal solution in contact with lesion in guttural pouch. 23.5: Recheck endoscopy of GP- resolution of fungal plaque, mild hyperaemia in area of previous infection

Case 23 Guttural pouch disease p2

• Follow up/ discussion
• Location of lesion in this case (not close to artery)- seemed unlikely that arterial occlusion would be of benefit.
• Previous case- deep fungal plaque over the mid-region of the stylohyoid bone- brown nasal discharge as only clinical sign- arterial ligation successfully resolved the lesion after 2wks topical clotrimazole had been unsuccessful.
• Current case- enilconazole solution infused into the pouch BID, horse cross-tied with head in neutral position for 30minutes after each infusion- maintain enilconazole solution in the pouch, in contact with lesion. Horse- complete recovery following 3 weeks tx in to GP, 6wks IM procaine penicillin for aspiration pneumonia.
• GP diseases- common. Most common include emphema and chondroids- usually caused by Strep. equi equi infections and mycosis- cause either haemorrhage, dysphagia, less commonly chronic nasal discharge. Neoplasia- occur in older horses.
• Several CNs course through GP- CN IX (glossopharyngeal_ , CN X (vagus), sympathetic nerves most commonly diseased by fungal plaques. Rarely damaged by bacterial infections (even severe ones),
• Clinical signs- associated with damage to CNs IX/X- dysphagia, laryngeal paralysis, soft palate displacement.
• Prognosis- grave if dysphagia is severe. Dysphagia - mild (fungal injury damaged only a branch of the vagus nerve).

Case 24 - Hypertrophic osteopathy

• 5yo Thoroughbred-Warmblood gelding. Intermittent fever for several weeks (as high as 39.7), weight loss of 6 months, developed bony swellings on distal radii/ tibias in last 2 weeks.
• PE- normal HR, increased RR (24). Chest auscultation- normal, no nasal discharge, no cough elicited. No enlarged lymph nodes. Mild circumlimbal oedema- both eyes, no evidence of uveitis. Limb palpation- marked enlargement of mid-left metacarpus metaphyses and diaphyses. Horse- not painful on palpation, nor lame at trot.
• Next diagnostic test- Limb radiography
• Most likely diagnosis- Hypertrophic osteopathy
• What should be done next- U/S chest (increased RR)
• What did it show- Several areas of pulmonary parenchymal consolidation (lack of aeration) on both sides in the mid-chest.
• Multiple lung lesions, fever, weight loss, lymphopenia, elevated fibrinogen suggests what pulmonary disease - Equine multinodular pulmonary fibrosis/ neoplasia. Multiple areas of consolidation in mid-thorax- pneumonia less likely, still possible (bacterial/ fungal)
• Confirm diagnosis - Transtracheal wash, BAL. Lung biopsy- previous tests undiagnostic. Transtracheal wash -histiocytic inflammation. Lung biopsy -moderate, locally extensive fibrosis. Negative for EHV-5 on PCR.
• How to treat- Corticosteroids (dexamethasone 0.1mg/kg every day, gradually tapering dose over 40days)
• Follow up/discussion
• Horse not given valacyclovir - negative EHV-5 testing. Treated with topical cidofovir in both eyes. Fever quickly resolved - corticosteroid treatment, made remarkable recovery- resolution of u/s abnormalities in the lung. Bony lesions did not resolve- remained sound.

Case 25- Tarsal valgus deformities

• Signalment- 36hr premature Arabian colt, treated for pneumonia and sepsis - failure of passive transfer. Marked leukopenia, neutropenia with toxic changes, lymphopenia and thrombocytopenia. Blood ACTH and cortisol levels- above the normal range- hypothalamus/pituitary/adrenal axis has responded appropriately to the illness. Mild symmetrical distension of carpal, tarsal and fetlock joints was noted. Day 3- foal unable to stand, no lameness. Radiograph of right tarsus was obtained- left was normal.
• Foal responded well to medical tx for pneumonia- discharged, told to limit exercise, maintained on good footing at home. Re-examined 1 month later for angular limb deformity. Radiograph of right tarsus again.
• Foal discharged, confined to small dirt stall- owners help him up hourly until comfortable to do so by himself. Omeprazole tx continued. Cast change every 2 weeks- after 2 cast changes improvement was shown, moved to grass paddock for rest of the year- no further tx. Re-examined at 4 months old, radiographs taken of the hocks. Sound at walk and trot.
• What does radiograph demonstrate - Incomplete ossification of tarsal bones. SMall tarsal bones and distal epiphysis of tibia slightly small and round.
• Shown in new radiograph - Tarsal valgus (was bilateral, right side more severely affected). Tarsus/ metatarsus- laterally deviated. Lateral tarsocrural joint space- abnormally wide, proximal aspect of lateral trochlear ridge is not distinct. Patchy decrease in bone opacity- seen in distal tibial epiphysis and metaphysis- physis was questionably wide. Due to asymmetrical growth in distal tibia- physitis/ epiphysitis and/ or asymmetrical ossification of tarsal and tibial bones.
• Recommended treatment- Bilateral sleeve casts applied from above the tarsus down to the fetlocks. Don't incorporate hooves. Legs- physically straightened as cast is applied. Foal- under GA (short acting) for cast placement.
• Most likely diagnosis and recommended treatment (x-rays)- Distal tibial metaphysis and epiphysis- normal size, shape and opacity. Distal tibial physis- improved, minimally wide and irregular medially. Lateral trochlear ridge- shorter than medial, improved from previous films. No thickening of soft tissues. Due to improvement, lack of lameness and O didn't want to sell/show foal- transphyseal bridging of distal tibia not recommended.

Case 25- valgus limb deformity

Case 26 - Pigmented urine

• 18month old Percheron gelding- evaluation of acute respiratory distress and dark coloured urine. Paddock mate- similar symptoms in previous 24hrs and then found dead.
• Evaluation- horse was dull, pale/grey mm. Tachycardic, tachhypnoeic, febril. Stream of black urine passed during examination.
• Diagnostic tests for urine discolouration - Discolouration occurs when abnormal pigments are present in the blood and filtered by the kidney. Common causes of pigmenturia- haemoglobin, myoglobin, frank blood, bilirubin. Assess serum - determine haemoglobinaemia or hyperbilirubinaemia is present. Urine dipstick - protein, blood or bilirubin- won't differentiate between haemoglobin and myoglobin. Spin the urine- determine if haemorrhage or pigmentation is present (RBC's spin down, pigment doesn't).
• Likely cause of the problem - Serum was haemolysed, severe anaemia present (PVC- 11%). Haemolytic anaemia- secondary to oxidative, infectious, immune-mediated, iatrogenic causes. Further discussion with the owner's - cause identified--> exposure to fallen branches of a red maple tree and ingestion of wilted leaves.
• Secondary problems when treating this case- Oxidative damage caused by toxic compounds in maple leaves- cause methaemoglobinaemia, result in sudden death due to hypoxia. Acute tubular necrosis caused by pigmenturia--> AKI. Severe haemolytic anaemia - DIC, activation of coagulation cascade by inflammatory mediators. Other complications - laminitis, organ damage due to hypoxia.

Case 27- ventricular tachycardia

• 3 yo Appaloosa gelding- examined due to fever (44oC), mild pectoral oedema w/o other signs. Treated with flunixin meglumine (500mg IV once)., 5 day TMPs (20mg/kg PO q12hr). Febrile episodes continued/ after 10 days- treated with K penicillen, gentamicin and metronidazole. Coggin's test for equine infectious anaemia- negative. 8 other adult horses on yard, no new inmates in last 6 months. After 3 days abx - fever still present.
• Intitial hospital examination - horse bright and alert, temp 38.7, RR24, HR 56, 2/6 diastolic murmur over aortic area. Thin horse BCS 3/9. Had lost weight/ muscle mass over past 2 weeks. Pitting, non-painful oedema over sternal area and prepuce.
• Horse treated with flunixin for 1 day symptomatic tx of fever. After 36hr- fever/ tachycardia persisted. Tentative diagnosis- immune mediated/ viral myositis/myocarditis (lack of evidence of bacterial infection)- tx dexamethasone. Become afebrile after 12hrs, tachycardia persisted (52-56), had significant tachycardia (>180), some distress and jugular pulses within 1 hr of dex injection. ECG performed.
• Suspect myocardial involvement- test cardiac troponin I -elevated. Echo performed.
• DDx for horse- Endocarditis, thoracic or abdominal abscess, purpura haemorrhagica, neoplasia.
• Additional diagnostics - U/S chest and abdomen (unremarkable), Rectal (unremarkable). CBC- mature neutrophilia. Biochemistry- mild decrease in albumin, low iron, marked increase in muscle enzymes. Transtracheal wash and peritoneal tap - unremarkable- Aspergillus fumigates cultured from wash. No known exposure to strangles- purpura haemorrhagica remained differential - submitted for Strep equi equi titre (moderately positive). Blood culture- no growth.
• ECG abnormality- Uniform ventricular tachycardia.
• Does arrhythmia need treating- what to treat with - Tx attempted due to tachycardia (high HR)- signs of cardiac compromise. Common tx- magnesium sulfate IV over 20 minutes or lidocaine administered IV with aim to revert to sinus tachycardia.
• Echocardiogram- Tachycardia, mild aortic valve thickening, decreased fractional shortening of left ventricle (20%). All diastole chamber- wnl.

Case 27 ventricular tachycardia p2

• Follow up/ discussion
• Myocarditis - not a rare disease in the horse - consider in horses with fever, tachycardia, elevations in muscle enzymes.
• Ventricular arrhythmias develop in some cases- life threatening.
• Cause of fever, myocarditis, skeletal myopathy- unproven: influenza, EHV-1, streptococcal myopathy, purpura-like syndrome, babesiosis, African horse sickness, anaplasmosis- all be considered.
• Increases in blood cTnI- specific for myocardial injury. Myocarditis -high levels, measurement important in both diagnosis and management.
• Ventricular arrhythmias/ other primary cardiac diseases may have normal or abnormal cTnI levels- helpful to measure in clinical management of the cases to determine need for corticosteroid tx/period of rest.
• Acute severe hypoxia or systemic inflammation- marked elevations of cTnI, corresponds to severity of illness. Changes in cTnI following tx more important in critically ill horses.
• Tx of myocarditis- relies on anti-inflammatories and corticosteroids- rapid decrease in fever, HR and cTnI concentration. Improvement in function should be seen- lowered HR, improved fractional shortening on echo.

Case 28

• 36hr old Warmblood filly- failure to urinate since birth, mild colic. Received 1 ml flunixin in muscle of RHL- tx sucralfate. Presentation-