Fibrocartilaginous Embolism
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Zinc Poisoning

(“FCE”)

Imagine your dog is happily playing in the yard, jumps up to catch a ball, lands badly, and comes up not just lame but not really able to use a back leg normally at all.  The toes knuckle under, perhaps. Maybe he sort tilts downward unable to rise all the way up in the back end.  You check him over, trying to find where it hurts and it simply does not seem to hurt at all.

There are many conditions that might fit here but the neurologic knuckling and the absence of a tender spot, suggests FCE.

SO WHAT IS “FCE” ANYWAY?

To understand FCE, one has to understand some anatomy of the vertebral column. The vertebral column consists of numerous small bones called “vertebrae” which are linked together by special joints called “intervertebral discs.” The discs are similar to the joints that connect arm or leg bones together in many ways. They allow flexibility between vertebrae so that one can arch or twist one’s back voluntarily just as one can flex and extend a knee or elbow.

But the discs are unique as well.  A joint of the appendicular skeleton, say a knee or elbow, has a capsule which secretes a lubricating fluid. The bones are capped with smooth cartilage to facilitate frictionless gliding as the surfaces move during flexion and extension. The disc is nothing like this. It is more like a cushion between the end plates of the vertebrae.  It is round (hence the name “disc”) and fibrous on the outside with a soft gelatinous inside to absorb the forces to which the bones are exposed. This jelly-like inside material inside is called the “nucleus pulposus” and it is the is material that makes up the fibrocartilaginous embolus.

The vertebral column provides a bony protective case around the vulnerable spinal cord. The spinal cord is the cable of nerve connections that transmits messages to and from the brain and controls the reflexes of the body.  The spinal cord is fed by a network of spinal arteries. In FCE, somehow the material from the nucleus pulposus enters the arterial system and is carried to the spinal cord where it causes a blood vessel obstruction: an “embolism.” This area of the spinal cord actually dies.  The process is not painful but generally recovery is not likely. Whatever neurologic loss has occurred within the first 24 hours, is likely to be permanent (though at least the condition does not get progressively worse.)

There are many theories of how disc material might gain access to the arterial blood supply but no one really knows how this happens.

THE TYPICAL PATIENT

Any dog can be a victim of FCE though about half of the victims are giant breed dogs.  Breeds that are called “chondrodystophic” (meaning they have as part of their normal breed conformation dwarf-like characteristics) tend to calcify their disc material, making it too hard to participate in an FCE and they are thus at lower risk. Such breeds include Basset hounds, and Dachshunds. Instead, these breeds tend to get Type I Disc Herniation, a different spinal problem but one at least amenable to surgery. Some feel the  Miniature Schnauzer has higher risk as this breed tends to circulate excess blood fats and cholesterol which may predispose to embolism.

Most FCE dogs are young adults, between the ages of 3 and 6 years.   In one study, 61% were presented for evaluation after some kind exercise injury or trauma. There may be a yelp at the time of the trauma but the injury is generally not painful. There is about a 50:50 chance that the lumbar area of the spinal cord will be affected which means only the rear legs will be involved.  Because the embolism is not generally a symmetrical event, both left and right may not be equally affected.

WILL MY DOG BE OKAY?

This depends on how much loss of function there is. The good news is that the loss of function will not get worse; after the first 24 hours, the maximum function loss has occurred. Your dog may or may not be able to improve (about 74% of dogs in one study showed some improvement ultimately) but be prepared for no improvement and ask yourself what kind of care will be needed and can your dog get around. Maximum improvement has generally occurred by 2 weeks after the time of the injury.

Many dogs are completely paralyzed. For more information on the care of the paralyzed dog click here.

Many dogs are simply weak in the affected limbs. They may or may not need assistance in getting around. It all depends on how severe the embolism was and where in the spinal cord it occurred.

HOW CAN WE BE SURE THIS WAS FCE?

Acute neurologic weakness after trauma could also be caused by Type I Disc Herniation or by spinal cord trauma. In Type I Disc Herniation, a mineralized intervertebral disc “slips” upward and is pressing on the spinal cord. The pressure may be relieved with medication (if it is not severe) or surgery may be needed. In either case, the spot where the disc is pressing is very painful. Beyond this, radiographic abnormalities may be seen when the patient’s back is radiographed.

In some cases, the collapsed disc spaces are not obvious and more advanced spinal cord imaging is needed. A myelogram involves general anesthesia and injecting special dye in the space around the spinal cord. If there is an area of compression, it will be visible and the patient can then proceed to surgery. In FCE, there is no such compression.

As for acute spinal cord trauma, it may not be apparent whether this has occurred versus FCE. If the lesion is acute, it is not unreasonable to treat it as an acute spinal injury and see if improvement results.

Magnetic Resonance Imaging (MRI) is not yet readily available to most veterinary practices but is likely to become the imaging modality of choice for the diagnosis of FCE. MRI is able to distinguish embolized areas of spinal cord from those with swelling or compression.  At this time FCE cannot be absolutely confirmed prior to death.