EQUINE VETERINARY EDUCATION / AE / MAY 2019


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previous history of S. equi infection (or any other respiratory disease) or vaccination for S. equi. No recent management changes were made. Diet consisted of brome hay supplemented with concentrate (Equine Strategy PurinaTM On the day of presentation, the mare was reported to


).


have a reduced appetite. Urination and faecal production were reportedly normal. Shared troughs made water consumption difficult to assess. With the exception of the phenylbutazone and ceftiofur crystalline free acid, the mare had not received other medications in the previous 60 days. Due to a failure to respond to initial medical therapy, the


progressive nature of proximal limb swelling and severe lameness, the mare was referred to the KSU-VHC for further diagnostic evaluation and therapeutic management. At presentation, the mare was quiet, alert and responsive.


The predominant abnormalities involved were marked lameness (4/5 AAEP) and severe swelling of the left hindlimb. Swelling extended from the level of the fetlock proximally to the stifle, with the most notable area of swelling from the tarsus to just above the stifle(Fig 1). Superficial abrasions were present on the distal aspect of the affected limb near the pastern. Digital pulses were normal. Vital parameters included a mild hyperthermia (rectal temperature 38.6°C), a normal heart rate of 42 beats/min, as well as an elevated respiratory rate (32 breaths/min). Body condition was considered good with a score of 5/9. Peripheral lymph nodes palpated normally. Oral mucous membranes were pink and moist with no evidence of petechial or ecchymotic haemorrhages. The remainder of the physical examination was unremarkable. Initial diagnostics revealed packed cell volume and total


protein to be 27% and 63 g/L, respectively. Ultrasonography of all affected oedematous structures involving the left hindlimb and ventral abdomen confirmed the presence of marked subcutaneous oedema. In most areas, the depth of


oedematous tissues measured approximately 3 cm. The diffuse and marked oedema, which was warm and painful to touch, was most consistent with septic cellulitis. Since there were no open wounds or draining tracks, fine needle aspirate of an affected area over the abaxial aspect of the mid-tibial region was performed. The sample was submitted for aerobic and anaerobic bacterial culture, as well as antimicrobial sensitivity testing. Based on the problems that included severe lameness,


marked oedema, fever, increased respiratory rate, anaemia and mild hypoproteinaemia, the working diagnosis was septic cellulitis. Treatment goals were aimed at resolution of the likely septic component of her disease and control of pain and inflammation. Phenylbutazone2 (2 mg/kg bwt i.v. q. 24 h) was continued for anti-inflammatory and analgesic purposes. Antibiotic therapy included oxytetracycline3 (6.6 mg/kg bwt i.v q. 12 h), and was selected based on broad spectrum coverage and favourable tissue penetration. Hydrotherapy was performed on the affected limb for approximately 20 min twice daily. This was followed by the application of topical 60% magnesium sulfate (Mag-60 Paste4) and plastic wrap with a support bandage to complete a sweat wrap that was left in place for approximately 12 h at a time. Hydrotherapy and bandaging were repeated daily for the duration of hospitalisation.


Diagnostics and case management


Over the subsequent 24 h (Days 1–2), the mare demonstrated marked deterioration in condition evidenced by profound lethargy, anorexia and marked icterus, as well as worsening of the oedema and lameness. Oedema of the left hindlimb had extended distally to include the fetlock but had also progressed to involve the ventral abdomen from the inguinal region and extended cranially to the axilla (Fig 2). She was also nonweightbearing when standing (grade 5/5) and was reluctant to flex the left hindlimb when ambulating resulting in dragging of the limb. It was suspected that the disease progression was a reflection of the primary disease originating in the left hindlimb and now extending to other adjacent areas. Repeated ultrasonographic evaluation revealed the ventral abdominal plaque of oedema tomeasure approximately 5 cm in depth in a diffuse manner along the affected ventral region. Additional evidence of clinical deterioration included marked tachycardia (60–80 beats/min) and development of pigmenturia (haeme positive on urine dipstick). Anaemia worsened over the initial 24 h post presentation evidenced by a PCV of 13% and total protein of 63 g/L (Fig 3). These findings suggested intravascular haemolysis, and upon gross haematologic evaluation, auto-agglutination of erythrocytes was evident. Serumbiochemistry revealed marked elevations of aspartate aminotransferase (AST 3695 U/L; rr 186–412) and creatine kinase (CK 131,760 U/L; rr 97–355) consistent with severe rhabdomyolysis (Fig 3). By Day 2 of hospitalisation, primary differentials included


Fig 1: Significant proximal limb oedema from the level of the proximal stifle to the hock was present in the left hindlimb on presentation.


infarctive purpura haemorrhagica, septic cellulitis and snake envenomation for the marked and progressive lameness, severe and asymmetric limb and ventral oedema and elevated muscle enzymes. There was no evidence of a snake bite that could be found on the affected limb. Immune-mediated haemolytic anaemia, as well as oxidative damage from toxins such as wild onion or Acer rubrum, were differential diagnoses for the acute and marked anaemia,


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