Long-term changes in gross body composition of paraplegic and quadriplegic patients

Abstract

INJURY to the spinal cord and the ensuing extensive paralysis of skeletal muscle is known to give rise to many metabolic changes (Cooper and Hoen, 1952; O'Connell and Gardner, 1953; Arieff et al., 1960). Some of these changes are generally reversible, such as the catabolic reaction resulting in marked loss of nitrogen, potassium and calcium (Cooper, et al., 1950), impairment of bromsulfalein clear ance (Cooper and Hoen, 1952) and development of gynecomastia in males. These abnormalities may disappear in the course of a few months, especially with modern treatment (Arieff et al., 1960). On the other hand, some changes seem to be essen tially permanent and these include disturbance of the distribution of serum proteins (Robinson, 1954; Arieff e t al., 1960), a tendency to creatinuria and decreased creatine tolerance (Pollock et at., 1954), a lowered excretion of creatinine and sub normal serum glutamic-oxalacetic transaminase levels (Arieff et al., 1960). The aim of the present work is to determine to what extent the gross body composition of spinal cord injured patients is altered as a result of such metabolic changes. The patients available in this hospital for the care and rehabilitation of the chronically ill were treated elsewhere during the acute post-injury phase. Consequently only the effects of relatively long-term metabolic changes would be apparent from these studies. In one approach, observations made on groups of paraplegic and quadriplegic patients were compared with those from groups of other chronically ill patients in this hospital in order to delineate differences specifically due to spinal cord injury. Comparison with data from the literature on healthy normal controls was also possible. In a second approach, in which the patient served as his own control, periodic observations were made on spinal cord injured subjects over a period of up to 51 months in order to follow changes in their body composition. Previous work on the variability in measurement of the selected parameters allowed assess ment of the statistical significance of the changes observed in the latter study (Greenway et al., 1965). METHODS Patient Selection. All patients were chronically ill, but in no acute distress. The spinal cord injured patients had no large decubitus ulcers and were all either 1 These studies have been supported in part by USPHS Grants A-1886, HD-00669 and VRA Grant RD-II44-M.

Salt wasting, hypotension, polydipsia, and hyponatremia and the level of spinal cord injury

“…20 Taking the first consideration, total water per body weight in the spinal cord injured subject is reportedly comparable to controls, but intracellular volume is diminished and extracellular volume is expanded (although intravascular volume is constricted). 17,21,22 Furthermore, the intracellular volume is more constricted in the tetraplegic than in the paraplegic subject, thus coinciding with the polydipsia of higher levels of paralysis in the current survey. The first mechanism, thirst induced by diminished intracellular volume, may apply to the spinal cord injured subject.…”

Gentamicin disposition kinetics in humans with spinal cord injury

“…The ratio of body fat to total body weight increases both in spinal man and in normals with ageing. These changes are seen earlier and are of a greater magnitude in spinal man suggesting that these changes are dependent on the pathophysiology of SCI and not the physio logical changes which normally accompany ageing, chronic illness or extended immobilization (Greenway et al, 1970).…”

“…This may be due to extensive erosion of muscle mass and other factors such as diminished peripheral venomotor tone contributing to the formation of subclinical oedema (Greenway et al, 1970;Bidart et al, 1971). The ratio of body fat to total body weight increases both in spinal man and in normals with ageing.…”

“…There exists a substantial body of knowledge defining the pathophysiology of SCI in humans (Greenway et al, 1970;Claus-Walker et ai., 1977) but essentially no knowledge concerning the extent to which this pathophysiology affects drug disposition kinetics and metabolism in spinal man (Livshits and Yakovlev, 1972;SSIE, 1983).…”

Cheyne–Stokes respiration, periodic circulation, and pulsus alternans in spinal cord injury patients

“…22 Reduction in breathing capacity may translate to reduction in venous return in general 23 and low cardiac output in tetraplegic patients in particular, 24,25 threatening medullary perfusion. A reduced blood volume occurs in some tetraplegic patients, indicated by hyponatremia, and can further reduce cardiac output and blood pressure, 26,27 compromising central circulation. Although this patient had a history of hyponatremia, serum sodium concentration was not determined at the time of monitoring.…”