232


EQUINE VETERINARY EDUCATION / AE / MAY 2019


Fig 2: Forty-eight hours after initial presentation, the mare developed pitting ventral oedema, extending approximately 5 cm below the abdominal wall, and was noted from the inguinal region to the axilla.


30 25 20 15 10 5 0


PCV CK


A 01 2 3 4 B 5 6


C 7


Day of hospitalisation


Fig 3: Graph depicting trends of creatine kinase and packed cell volume during hospitalisation. Dexamethasone (2 mg/mL) dosing is denoted by time points (A–D) Doses at each time point are as follows: (A) 0.2 mg/kg bwt i.v. q. 12h; (B) 0.1 mg/kg bwt i.v. q. 12 h; (C) 0.1 mg/kg bwt i.v. q. 24 h; (D) 0.1 mg/kg bwt i.m. q. 24 h.


icterus, pigmenturia and tachycardia. IMHA can result from a primary immune response or be secondary to infectious aetiologies including equine infectious anaemia (EIA) and Clostridium perfringens, pharmacological agents including penicillin, or as a component of paraneoplastic syndrome to accompany neoplasia. Additional differential diagnoses for tachycardia included pain and myocarditis. Based on season (summer), history and clinical presentation including auto- agglutination, toxin ingestion was considered unlikely. Primary management goals were aimed at patient


stabilisation and elimination of the inciting pathogen. Serial serum chemistries revealed ongoing muscle damage, with CK values fluctuating between 60,000 and 148,000 U/L (Fig 3). The mare was placed on intravenous lactated Ringer’s solution at a rate of 60 mL/kg bwt/day 12 h after presentation as diuretic therapy for the elevated muscle enzymes and because the mare was not drinking adequately. Although marked pigmenturia was evident, renal injury secondary to myoglobinuria and/or haemoglobinuria was not apparent based on normal renal values, normal urine specific gravity (pre-IVFT USG) and urinalysis. In an effort to determine the cause of the marked


intravascular haemolysis and auto-agglutination noted on Day 2, erythrocyte surface immunoglobulin (SAIg) testing


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8 9 D


20,000 40,000 60,000 80,000 100,000 120,000 140,000 160,000


10 0


using direct immunofluorescence (Wilkerson et al. 2000) confirmed IMHA (IgG-coated erythrocytes 7%; rr <3%). While this result was not markedly elevated, with the presence of severe anaemia and gross erythrocyte agglutination, an abnormal result was consistent with the presence of surface-associated antibody and supported a diagnosis of IMHA. EIA testing was negative. Based on the severity of anaemia and progressive nature of haemolysis, major and minor cross matches were performed on four KSU College of Veterinary Medicine owned horses 36 h after initial presentation (Day 2). Among the horses tested, there was some reaction between patient and all available donor horses for both major and minor cross match testing. These reactions were consistent with the pronounced level of immune activation that the recipient demonstrated clinically. The least reactive cross match was a major 2+ and minor 1+. Even though there were concerns of a potential transfusion reaction, the mare was in critical condition and the need for increased tissue oxygen delivery was considered urgent. In addition, the mare received 0.2 mg/kg dose of


dexamethasone2 (2 mg/mL) to ameliorate ongoing and potential worsening immune-mediated erythrocyte destruction and vasculitis, and 8 L of whole blood was administered approximately 40 h after presentation. The mare did not demonstrate evidence of acute or delayed transfusion reactions. Following whole blood transfusion, PCV rose and stayed above 18% for the remainder of hospitalisation. Due to persistent tachycardia (60–80 beats/min) and development of an irregular cardiac rhythm on Day 3 of hospitalisation, an ECG was performed which revealed ventricular premature complexes. Echocardiographic examination was unremarkable. Cardiac troponin I levels were significantly elevated at 41.83 ng/mL (rr 0–0.7), supporting the diagnosis of myocarditis. Based on the fact that the most common aetiologic


agent associated with purpura haemorrhagica is S. equi, diagnostics were aimed at determining if this pathogen was playing a role in disease manifestation. Streptococcus equi subspecies equi M protein (SeM) ELISA titre, upper airway endoscopy, rectal palpation, thoracic and abdominal ultrasound were performed on Day 4. Streptococcus equi subspecies equi M protein titre was negative (<1:200). Upper airway endoscopy was within normal limits, ruling out chondroids or guttural pouch empyema associated with


PCV (%)


Creatine kinase (U/l)


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