Postural hypotension, hyponatremia, and salt and water intake: case reports.

PURPOSE: Postural hypotension (PH) and hyponatremia are common and often coexistent among patients with severe paralysis secondary to spinal cord injury. Volume depletion could account for these conditions. This study examined whether salt and water intake correlated with the severity of PH. PARTICIPANTS: Participants were 4 patients with tetraplegia, motor and sensory complete, aged 68 to 83 years, who were paralyzed for 9 to 54 years, who had PH. These patients were ranked by the amount of ephedrine prescribed on a daily basis to treat PH over the preceding 2-year period. METHODS: The total urinary output of sodium and water and the effect of orthostasis on urine output rate, osmolality, sodium concentration, and creatinine secretion were determined over a 48-hour period of collection and compared with severity of PH. RESULTS: The ephedrine requirements, in order of decreasing severity of PH, were 100 mg/d, 25 mg/d, 12.5 mg/d, and no ephedrine needed. The 24-hour sodium excretions in that order were 50, 92, 180, and 164 mEq. The urine volumes were 1.4, 3, 2.6, and 5.4 L, respectively. In the same order of decreasing PH severity, the sitting position relative to the recumbent position was characterized by increasing rates of creatinine secretion (ratios of 0.69, 0.74, 0.95, and 0.80), increasing rates of water excretion (ratios of 0.49, 0.28, 0.69, and 0.99), decreasing urine osmolality (ratios of 1.2, 1.8, 1.3, and 0.8), and increasing sodium concentrations (ratios of 0.9, 1.3, 1.2, and 2.6). CONCLUSION: In these individuals with tetraplegia, severe PH was accompanied by avid conservation of water and impaired retention of sodium in the sitting position, as well as limited salt and water intake.

[The coincidence of acute intermittent porphyria and Crohn's disease]. / Koinzidenz von akuter intermittierender Porphyrie und Morbus Crohn.

In the course of four weeks, tetraparesis developed in a 28-year-old man with Crohn's disease for the last six years, treated with glucocorticoids and sulphasalazine. The cause was acute intermittent porphyria which had been previously overlooked because of the similar abdominal symptoms of Crohn's disease. Treatment with glucose, propranolol and haemarginate failed to bring about any improvement, but there was a remission of the porphyria. This case demonstrates that diagnosis of acute intermittent porphyria in the presence of Crohn's disease is difficult, and if delayed therapeutic measures in the face of persisting neurological complications are of little benefit.

Hyponatraemia in quadriplegic patients.

1. Studies were performed in five hyponatraemic (plasma sodium 129 +/- 1.6 mmol/l; plasma osmolality 268 +/- 3.0 mosmol/kg) quadriplegic patients in order to elucidate its aetiology. Five age- and sex-matched healthy subjects served as controls. 2. Daily urine volumes were high (4454 +/- 624 ml) in the quadriplegic patients secondary to habitually increased fluid intake. 3. All quadriplegic patients had suppressed plasma arginine vasopressin levels (less than 0.8 pmol/l) and were able to form dilute urine after a water load (20 ml/kg). However, free water clearance and the ability to excrete the water load were frequently impaired, and these defects were associated with reductions in both osmolar clearance and delivery of filtrate to the distal diluting sites of the nephron. 4. During hypertonic saline (5%, w/v, NaCl) infusion, plasma arginine vasopressin rose progressively before plasma osmolality reached the normal range, consistent with a resetting of the osmostat. 5. We conclude that hyponatraemia in quadriplegic patients is related to an intrarenal defect in water excretion and resetting of the osmostat coupled with increased fluid intake.

Haemodynamic, hormonal and urinary responses to postural change in tetraplegic and paraplegic man.

We have studied the haemodynamic, hormonal and urinary effects of postural change in 6 tetraplegic patients, 6 paraplegic patients and 6 normal subjects. Measurements of blood pressure and heart rate, plasma renin activity, plasma aldosterone, urine volume and electrolyte excretion were made for 60 minutes while sitting and 60 minutes while recumbent. In tetraplegics the blood pressure was lower when sitting and rose during recumbency, unlike paraplegics and normal subjects. Plasma renin activity and aldosterone were higher in tetraplegics when sitting compared to normal subjects and did not fall during recumbency. Urine output increased significantly after recumbency in tetraplegics, but not in paraplegics or normal subjects. Both urinary sodium and potassium excretion were lower in tetraplegics and higher in paraplegics compared to normal subjects when sitting. In paraplegics the fall in both sodium and potassium excretion did not appear to be related to change in posture. Our observations indicate that recumbency induces a diuresis in tetraplegics but not in paraplegics or in normal subjects. The diuresis in tetraplegics may be related to the accompanying haemodynamic and hormonal changes induced by recumbency.

Urinary elimination of glycosaminoglycans during the immobilization osteoporosis of spinal cord injury patients.

Urinary glycosaminoglycans (GAGs) were measured in 47 paraplegics, six tetraplegics, and ten control subjects. In two paraplegics, the GAG rates were compared with those of hydroxyprolinuria and calciuria during one year. The GAG excretion rate found during the first five months after spinal cord injury increased significantly, up to three or four times the normal rate. No significant differences were found between paraplegics and tetraplegics. This increase in glycosaminoglycanuria parallels the previously reported increase in hydroxyprolinuria. The formation of a neurogenic paraosteoarthropathy showed the highest increase in hydroxyprolinuria. These biochemical assessments reflect the modifications in the bone matrix and cutaneous tissue associated with immobilization osteoporosis in spinal cord injury patients.

Increased urine calcium during hyperalimentation in quadriplegia: report of 2 cases.

Two acute quadriplegic adolescent boys with hypercalcemia had large increases in urine calcium during calcium-free, or nearly free, intravenous hyperalimentation. The calcium which spilled in the urine proved to be of endogenous origin since it was accompanied by proportional amounts of hydroxyproline. To limit the endogenous bone losses during hyperalimentation, it is recommended that calcium in an amount equal to that loss be added to the perfusate so that only exogenous calcium is spilled in the urine.

Free amino acid excretion in tetraplegic patients.

Free amino acid chromatographic fingerprints obtained in automated analysers in 24-hour urines may help to quantitate muscle and collagen changes occurring after cerival spinal cord injury. The technique was used to compare the urine of six healthy and ten tetraplegic men, 18 to 25 years old, three of whom became paralysed in diving, one in a mountain fall, one one in the fall of a pipe, four in car accidents, and one in a football game. Nine weeks to 14 years after injury, the tetraplegics excreted less total free amino acids, lysine, and 3-methylhistidine than the controls, whereas hydroxyproline and hydroxylysine were similar in both groups. Values of urine 3-methylhistidine, measured 9, 13, 19 and 20 weeks post onset in one patient, and 9, 12, 16, 18, 23, and 26 weeks post onset in another, were related to the duration of paralysis. These results indicate that collagen and muscle metabolism may not be quantitated by measuring urine free amino acids.

Mineral metabolism in spinal cord injury.

In 10 paraplegic and 10 quadroplegic subjects, bone resorption was investigated by determining urinary excretion of hydroxyproline, calcium, and phosphorus. Measurements were performed weekly from the onset to 4 months after injury. During the first 7 weeks following injury, urinary excretion of calcium in paraplegic and quadriplegic subjects reached the highest level (380 +/- 180 mg/24hr). From 7 to 16 weeks after injury average urinary excretion of calcium (245 +/- 72 mg/24hr) remained significantly greater than that in controls (100 +/- 25 mg/24hr; p less than 0.05). Urinary hydroxyproline was elevated in paraplegic subjects (80 +/- 18 mg/24hr) for 8 weeks and in quadriplegic subjects (102 +/- 37 mg/24hr) for the entire 16 weeks following injury compared with that in controls (48 +/- 12 mg/24hr; p less than 0.05). Both paraplegic and quadriplegic subjects excreted more phosphorus (1.6 +/- 0.4 gm/24hr) than controls (0.85 +/- 0.2 gm/24hr; p less than 0.05) only during the first 2 weeks following spinal cord injury. During the acute phase of the injury (0-3 months), urinary excretion of calcium and magnesium was significantly higher (p less than 0.05) in subjects with complete compared with incomplete spinal cord lesions.

Cervical spinal cord lesions disrupt the rhythm in human melatonin excretion.

To determine whether spinal cord lesions disrupt the diurnal activity of the human pineal, urinary melatonin levels were measured over 24 hours (4 or 8-hourly intervals) in male patients with clinical evidence of cervical spinal cord transection. During the waking state, levels of melatonin in these subjects ranged from 3.2--13.5 ng/4 hours; during sleep and darkness, values ranged from 1.8--10.5 ng/4 hours. Levels of serum cortisol, aldosterone, and growth hormone showed rhythmic variations in these subjects. The absence of significant nocturnal melatonin increases distinguishes quadriplegic subjects from normal males and from one subject with a lesion of the lumbar spinal cord. These differences may be caused by "decentralization" of the pineal organ due to a lesion within the cervical spinal cord interrupting descending sympathetic fibers. If so, the human pineal, like that of other mammals, is regulated, at least in part, by activity within the central nervous system via sympathetic nervous connections.

Immediate endocrine and metabolic consequences of traumatic quadriplegia in a young woman.

Onset of paralysis by cervical spinal cord injury led immediately to temporary adrenocortical activation and, within 2 days, to sustained skin and bone breakdown. Urine cAMP was increased, blood parathyroid hormone, renin activity, and electrolytes were normal, and fluid and electrolytes balance became negative during the initial 6 days of paralysis.

The urinary excretion of collagen degradation products by quadriplegic patients and during weightlessness.

Urinary total hydroxyproline, peptide-bound hydroxyproline, hydroxylysine glycosides, and calcium were measured in three healthy individuals subjected to weightlessness for eighty-four days and in three young quadriplegic patients. The former group had significant calciuria but no evidence of collagen degradation. The latter group, however, had conspicuous calciuria and also excreted large amounts of collagen breakdown products. This documented degradation of matrix may be related to the continuous calciuria, osteoporosis, and cutaneous dystrophic changes occurring in quadriplegics.