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EQUINE VETERINARY EDUCATION
Equine vet. Educ. (2022) 34 (7) 346 doi: 10.1111/eve.13522_1
Case Report
Complete AV block in a neonatal foal suffering from nutritional myodegeneration
T. M. Conze†*, A. Falkenau‡, L. S. Goehring† and A. May† †Equine Hospital, Ludwig-Maximilians University, Munich and ‡Institute of Veterinary Pathology, Ludwig-Maximilians University, Munich, Germany *Corresponding author email:
theresa.maria@
gmx.de
Keywords: horse; nutritional myodegeneration; white muscle disease; complete AV block; dysrhythmia; selenium
Summary This case report is about a 1-day-old, full-term Quarter Horse colt presented for progressive inability to rise and nurse. Besides the general weakness, a marked bradycardia was evident. The blood work revealed markedly increased muscle enzymes, azotaemia, hypoproteinaemia and hyperlactataemia, as well as hyponatraemia, hypochloraemia, acidosis and hypoxaemia. Blood samples also yielded low concentrations of selenium and vitamin E and an elevated troponin I value. An ECG revealed complete atrioventricular (AV) dissociation (Fig 1). The low ventricular escape rhythm was regular with monomorphic QRS complexes. Occasionally, ventricular premature beats of bizarre, widened shape occurred, suggesting additional ectopic foci somewhere else in the ventricle. An echocardiographic examination showed no congenital cardiac defects and revealed only mild alterations in cardiac dimensionswhichmainly reflected compensatory mechanisms to increase ventricular stroke volume and thereby cardiac output. Subsequently, the diagnosis of acute nutritional myodegeneration (NMD) was
made based on clinical signs, elevated muscle enzymes, ECG findings, as well as low serum selenium and vitamin E values. The complete AV block and slow ventricular escape rhythm was attributed to damage of the myocardium involving the conduction pathways. Despite intensive care and supportive therapy with intravenous fluids, anti-inflammatory drugs, and antimicrobials, as well as selenium and vitamin E substitution, the foal´s condition deteriorated. Administration of parasympatholytic and sympathomimetic drugs did not result in a significant increase in heart rate orAV conduction.Due to the poor prognosis and the
Fig 2: Right ventricle (H&E stain, scalebar = 100 µm): Purkinje fibres display intracellular mineralisation (arrow) as well as
fragmentation of cytoplasm (arrowhead) and resorptive cellular infiltrates as seen in skeletal and cardiac myocytes (not shown).
lack of response to intensive therapy, the owner elected euthanasia. Necropsy confirmed the diagnosis of NMD and revealed diffuse necrosis and resorptive cell infiltration of the
skeletal and myocardial musculature. Apart from these typical findings, multifocal degeneration and even mineralisation of Purkinje fibres (Fig 2), as a part of the cardiac conduction system, were detected and might have caused complete AV block and ventricular ectopy. Prevention of NMD is the key since treatment of the acute form is often unsuccessful as shown in the present case. Therefore, the selenium status of the dam should be monitored throughout the gestation period, especially in regions with selenium-deficient soils.
Key points
• Due to unspecific clinical signs, like weakness and dysphagia, NMD needs to be differentiated from other diseases affecting young foals.
Fig 1: Modified base-apex ECG tracing of the 1-day-old foal. Complete AV-dissociation is evident and is identified by variable P-R intervals (blue double arrow). The atrial rate is about 120 beats/min with a lower ventricular rate of 24 beats/min. Black arrow = p-waves buried in QRS-T complexes. Paper speed = 50 mm/s, 1 mV = 20 mm.
• Dysrhythmia due to myocardial damage and degeneration of the cardiac conduction system in NMD foals may mask the underlying disease.
• Since the prognosis for foals suffering from acute NMD is poor, herd surveillance programs with selenium supplementation as required are paramount in selenium-deficient areas.
© 2021 EVJ Ltd
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