Thomas I. Hoen

Metabolic Disorders in Paraplegics

IT IS the purpose of this report to summarize briefly observations concerned with metabolic abnormalities observed in paraplegic patients. This review included clinical data on over 300 paraplegic patients studied during the past five years. The majority of these were paraplegic as a result of traumatic lesions of the spinal cord, and, except where otherwise indicated, this discussion deals specifically with traumatic paraplegics.

Decompression of the spinal cord in Pott's paraplegia☆

Abstract A case of Potts disease of the thoracic spine in a young girl has been reported. This patient became paraplegic after she was discharged from the hospital, asymptomatic, with solid spinal fusion. Re-exploration showed that the spinal fusion was intact, and lateral rachiotomy disclosed a bony ridge pressing backward upon the spinal cord. Removal of this ridge did not result in regression of the paraplegia until after an abscess had appeared on the surface, having apparently tracked up the path of the surgical procedure. The paraplegia then began to regress and the patient went on to make a complete recovery. This suggests that when the paraplegia does not subside rapidly after signs of healing or of good fusion, or when late paraplegia appears in the presence of a good fusion, exploration should be done and such abscess material as can be found should be removed. Antibiotics render such a procedure much safer than formerly. Our patient did not become paraplegic until she was ambulatory. It seems likely that despite the solid fusion weight bearing had forced some purulent material, which was formerly lying within the vertebral body, out into the canal space, with development of pressure on the cord and paraplegia.