Embolia fibrocartilaginosa

Fibrocartilaginous Infarction:

Even though animals do not suffer from to the same degree of vascular disease as human beings, infarction of the spinal cord with fibrocartilaginous material is not uncommon.
It occurs in any breed of dogs, but is most common in large breeds, such as Great Danes, Labrador retrievers and German Shepherds. Although both arteries and veins can be affected, most commonly it is the venous system of the spinal cord which is obstructed, leading to a hemorrhagic infarction.
It is believed that herniation of the nucleus pulposus takes place either into the vertebral body or the venous sinuses within the spinal column. Since the vertebral body represents a vascular space communicating with the spinal venous system, the material gains access to the spinal veins. These veins do not have valves, allowing the fibrocartilaginous material to flow up and down the spinal column. When intra-thoracic pressure increases, this material can be back-flushed into small penetrating spinal cord veins. When the intra-thoracic pressure returns to normal, the veins collapse trapping the material and leading to excessive venous pressure upstream to the occlusion. The venules rupture leading to a hemorrhagic infarction.
The pattern of infarction usually affects a quadrant of the spinal cord, although initial signs may affect more of the spinal pathways from inflammation and spinal cord swelling.
The infarction can occur anywhere along the spinal cord, but the causal cervical and mid- to lower lumbar spinal cord segments appear to be most frequently involved.
The presence of spinal cord infarction should be suspected whenever a patient presents with acute onset of paresis or paralysis which is markedly asymmetrical and there is no evidence of hyperpathia.
Vascular disease is generally acute and non-progressive. In addition, the spinal cord contains pain pathways, but no pain receptors. As such, strict diseases within the spinal cord without meningeal involvement are usually not painful. Most of the other diagnostic tests will be within normal limits.
Occasionally, there will be evidence of hemorrhage on CSF analysis. Spinal radiographs, do not demonstrate the disease, but may reveal other evidence of spinal column degeneration. Myelography will be normal or demonstrate mild intramedullary swelling. In a small number of cases (where the vascular occlusion is secondary to a systemic disease), the minimum data base will show evidence of the systemic disease.
The treatment of spinal cord infarction is that for acute spinal cord injury, using methylprednisolone at 30 mg/kg initially. This is followed by 15 mg/kg every 8 hours for the first 24-48 hours. Then, oral prednisolone is begun at 0.5 mg /kg every 12 hours for 5 days. I continue prednisolone at 0.5 mg/kg every other day, in the morning, for up to another 2 weeks.
Many cases will improve dramatically within the first week, although they will still improve over several months. If there has been no improvement in the first week, re-examination and additional tests may be indicated. Since usually only a quadrant of the spinal cord is affected, the patient will improve most on the unaffected side. Reorganization will usually allow these patients to function adequately. Spinal cord infarction from fibrocartilaginous material is a sporadic problem and, usually, does not reoccur.

Caso clínico de embolia fibrocartilagionosa en un boxer

Imágenes de su resonancia magnética

Fuente del texto: Universidad de Florida (USA)


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