A challenging case: Progressive, generalized pain in a young English bulldog - Veterinary Medicine
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A challenging case: Progressive, generalized pain in a young English bulldog
These clinicians identify the cause of a dog's extreme, difficult-to-localize pain and successfully alleviate it.


Pathophysiology and vertebral blood flow

In order to understand the pathophysiology involved in vertebral infections, knowledge of the vascular anatomy and blood flow of the vertebral column is needed. The vertebral venous system is a set of valveless vessels that carries blood under low pressures. It connects with and provides bypasses for the portal, pulmonary, and caval systems of veins and can provide a pathway for disease to spread among organs.19,20

The internal ventral vertebral venous plexus is made up of paired longitudinal valveless vessels that extend from the caudal vertebrae to the foramen magnum and course along the floor of the vertebral canal ventral to the spinal cord. Blood may flow cranially or caudally depending on pressure.19,21,22 The internal ventral vertebral venous plexus drains into the vertebral bodies where it joins the basivertebral veins. Venous blood exits the vertebral bodies via the basivertebral veins. The basivertebral veins join the internal ventral vertebral plexus with the external ventral vertebral plexus. In the lumbar region, the basivertebral veins are largest, and in this region they connect with lumbar veins by the ventral venous plexus.22 This arrangement may explain the frequent involvement of the lumbar region in vertebral physitis. The intervertebral veins anastomose the vertebral plexuses and extravertebral veins. These vessels drain the vertebral regions and are closely associated with surrounding organs.22 Hematogenous extension of infection or neoplasia occurs through connections with surrounding tissues.19-21,23 Retrograde flow in the vertebral veins may contribute to localization of infection or neoplasia in the vertebrae.5

Metastasis of malignancies involving the prostate, bladder, or uterus to the lumbar spine has been seen in human and veterinary medicine.24-31 In addition, infections such as pyelonephritis, perinephritis, prostatitis, and cystitis have preceded vertebral infections.24,26,32 In the 1940s, it was hypothesized that such patterns of metastasis and spread of infection were caused by an increase in intra-abdominal pressure that prevented blood flow from the pelvis to the inferior vena cava, causing shunting of the blood to the vertebral vein system.19,21 In the normal course of blood flow, radiopaque material injected into the dorsal vein of the penis of monkeys coursed to the inferior vena cava. However, with increased intra-abdominal pressure, the injected material ascended to the internal vertebral venous plexus rather than the vena cava.19,21

In rats and rabbits, tumor cells introduced into the femoral vein while intra-abdominal pressure was elevated bypassed the lungs and led to tumor growth in the lumbar vertebrae.33 Increased intra-abdominal pressure may occur in animals from activity such as coughing, sneezing, or straining to defecate.19

In vertebral physitis, the infection is thought to involve the highly vascular metaphyseal and epiphyseal capillary beds.2,34 Blood in this area flows relatively slowly, and the primary spongiosa lacks white blood cells, allowing bacterial colonization.35 In discospondylitis, the infection is thought to develop from the same epiphyseal capillaries with rapid diffusion of microorganisms into the avascular intervertebral disk and the adjacent vertebral end plates.2,4,35

Clinical and radiographic signs

Clinical signs of vertebral infections may include pain, fever, anorexia, lethargy, and neurologic deficits such as ataxia and paresis. The neurologic signs depend on the location and severity of the lesion.2,5 The most common clinical signs of vertebral physitis are spinal hyperesthesia, lethargy, and pelvic limb weakness.2

Early radiographic signs of vertebral physitis include widening and lucency of the caudal physis with loss of normal physeal margins. Later radiographic findings include a collapsed or narrowed physis surrounded by sclerosis and remodeling of the ventrocaudal region of the vertebra. Vertebral end plates are normal, and no changes are noted at the intervertebral disk space. These features distinguish vertebral physitis from discospondylitis.2,4


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