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Fibrocartilaginous embolism

ISSN 2398-2942

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Synonym(s): Fibrocartilaginous embolic neuropathy, Ischemic myelopathy, FCE

Introduction

  • Peracute onset disease, usually marked lateralization of deficits, although bilateral signs are often seen initially.
  • Cause:
    • Ischemic necrosis of spinal cord associated with fibrocartilaginous emboli in blood vessels.
    • Cervical and lumbar spinal cord enlargements commonly involved, but can occur anywhere along spinal cord.
  • Signs:
    • Peracute (<6 hours) onset of non-painful, non-progressive (after 24 hours) and often asymmetric myelopathy.
    • Reflect the location of the lesion. Can be UMN or LMN paresis/plegia.
  • Diagnosis: signs, myelography or CT/MRI scan to rule out spinal cord compression.
  • Treatment: mostly supportive care.
  • Prognosis:
    • Fair to good: if neurological signs are mild to moderate without profound LMN deficits.
    • Very poor to hopeless: with profound LMN signs with loss of pain sensation.
      Print off the owner factsheet Ischemic myelopathy Ischemic myelopathy to give to your client.

Presenting signs

  • Peracute onset.
  • Often associated with trauma or exercise.
  • Paresis and ataxia Ataxia.
  • Sudden onset initial pain which rapidly resolves.
  • Can be markedly asymmetrical or unilateral.
  • Spinal hyperesthesia can be present initially but is absent after the onset of ischemia.

Age predisposition

  • Any age group.
  • Been confirmed histologically in young (8-13 weeks of age) Irish Wolfhounds Irish Wolfhound.
  • Most are between 3-7 years.

Breed/Species predisposition

  • Frequently large, or giant (non-chondrodystrophic) breed.
  • Chondrodystrophoid breeds have a negligible incidence.

Cost considerations

  • Intensive care can be expensive.
  • Supportive care. This is a non-surgical disease.

Pathogenesis

Etiology

  • Mechanism unknown - embolism most commonly occurs in the spinal cord arteries, although can be associated with veins or both arteries and veins.
  • Fibrocartilaginous emboli thought to be intervertebral disk material (nucleus pulposus).
  • In very young animals growth plate cartilage is another possible source.
  • Possible increases in intra-abdominal pressure may alter blood flow dynamics and direction to the spine, intervetebral disks and spinal cord, allowing diskal embolization of the spinal cord to occur.

Predisposing factors

General
  • A very high percentage of dogs have been exercising at the time of the embolism.

Specific

  • Hyperlipoproteinemia Hyperlipidemia has been suggested to predispose to this condition in some breeds, eg Miniature Schnauzer and Shetland Sheepdog.

Pathophysiology

  • The ischemic injury caused by the arterial obstruction initiates a series of biochemical and metabolic events which result in neuronal and glial cell dath. The grey matter is affected more severely due to its greater metabolic demand.

Timecourse

  • Immediate onset following location of embolus.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Bartholomew K A, Stover K E, Olby N J et al (2016) Clinical characteristics of canine fibrocartilaginous embolic myelopathy (FCE): a systematic review of 393 cases (1973-2013). Vet Rec 179, 650 PubMed.
  • Fenn J, Dress R, Volk H A et al (2016) Inter- and Intraobserver agreement for diagnosing presumptive ischemic myelopathy and acute noncompressive nucleus pulposus extrusion in dogs using magnetic resonance imagingVet Radiol Ultrasound 57, 33-40 PubMed.
  • Fenn J, Drees R, Volk H A et al (2016) Comparison of clinical signs and outcomes between dogs with presumptive ischemic myelopathy and dogs with acute noncompressive nucleus pulposus extrusion.  JAVMA 249, 767-775 PubMed.
  • De Risio L, Platt S R (2010) Fibrocartilaginous embolic myelopathy in small animalsVet Clin North Am Small Anim Pract 40, 859-869 PubMed.
  • De Risio L, Adams V, Dennis R et al (2008) Association of clinical and magnetic resonance imaging findings with outcome in dogs suspected to have ischemic myelopathy: 50 cases (2000-2006). JAVMA 233, 129-135 PubMed.
  • De Risio L, Adams V, Dennis R et al (2007) Magnetic resonance imaging findings and clinical associations in 52 dogs with suspected ischemic myelopathy. J Vet Intern Med 21, 1290-1298 PubMed.
  • Ueno H, Shimizu J, Uzuka Y et al (2005) Fibrocartilaginous embolism in a chondrodystropoid breed dog.  Aust Vet J 83, 142-144 PubMed.
  • Gandini G, Cizinauska S, Lang J et al (2003) Fibrocartilaginous embolism in 75 dogs: clinical findings and factors influencing the recovery rate. J Small Anim Pract 44, 76-80 PubMed.
  • Junker K, van den Ingh T S, Bossard M M et al (2000) Fibrocartilaginosu embolism of the spinal cord (FCE) in juvenile Irish Wolfhounds. Vet Q 22, 154-146 PubMed.
  • Cauzinille L et al (1996) Fibrocartilaginous embolism of the spinal cord in dogs - review of 36 histologically confirmed cases and retrospective study of 26 suspected cases. J Vet Intern Med 10 (4), 241-245 PubMed.
  • Oliver J E (1993) What is your neurologic diagnosis? Infarction of spinal cord caused by fibrocartilaginous embolus. JAVMA 203 (1), 49-50 PubMed.
  • Doige C E et al (1983) Fibrocartilaginous embolism and ischemic myelopathy in a four month old German Shepherd Dog. Can J Comp Med 47 (4), 499-500 PubMed.
  • Gill C W (1979) Case report - fibrocartilaginous embolic myelopathy in a dog. Can Vet J 20 (10), 273-278 PubMed.

Other sources of information

  • Neer T M (1992) Fibrocartilaginous emboli. Vet Clin North Am Small Anim Pract 22(4), 1017-1026 (Review).
  • Cook J R Jr (1988) Fibrocartilaginous emboli. Vet Clin North Am Small Anim Pract 18(3), 581-592 (Review).