J R Silver1, J R Doggart. 1. National Spinal Injuries Centre, Stoke Mandeville Hospital, Aylesbury, Buckinghamshire, UK.
Abstract
STUDY DESIGN: Assessment of sodium output in spinal injury patients. OBJECTIVES: The purpose was to examine the effects of sodium loading acutely by an infusion, long term by sodium supplements, to acutely injured spinal patients on a fixed sodium intake. This was compared with another group of acutely injured patients who were on a hospital diet of between 50 and 150 mmol of sodium daily. SETTING: The National Spinal Injuries Centre, Stoke Mandeville Hospital, Aylesbury, Bucks HP21 8AL, UK. METHODS: A total of 53 studies were carried out on 52 patients between 1962 and 1964. In all, 49 patients were studied during the first 10 days after injury as follows: a control group of 39 patients received no supplementary sodium, two received NaCl infusion, two NaCl tablets orally, and six received NaCl infusion followed by NaCl tablets orally. Four patients were studied for more than 15 days after injury (one of these had been studied in the acute stage); they received NaCl infusion and one (42d) received in addition NaCl tablets for four subsequent days. RESULTS: In all patients urinary sodium excretion was minimal on day 2 and increased thereafter. On days 2-6, it was significantly lower in patients with a complete transection of the cervical cord than in patients with lower lesions. In the early studies, nine patients excreted less than 40% of the administered load within 24 h. In four of these patients excretion was 10% or less. In the later studies, three of the four patients excreted at least 80% of the infused Na+ on the same day. CONCLUSION: Sodium retention in the patient with cord injury is a response to trauma. The different responses seen in patients with different levels of cord transection are not due to direct changes in the innervation of the kidney but to compensation for sympathetic insufficiency, blood pressure being maintained by the secretion of aldosterone, vasopressin and other hormones. The decreased urinary output seen acutely after cord transection is not due to renal failure and the patient's condition can be made dangerously worse by attempts to create a diuresis.
STUDY DESIGN: Assessment of sodium output in spinal injurypatients. OBJECTIVES: The purpose was to examine the effects of sodium loading acutely by an infusion, long term by sodium supplements, to acutely injured spinal patients on a fixed sodium intake. This was compared with another group of acutely injured patients who were on a hospital diet of between 50 and 150 mmol of sodium daily. SETTING: The National Spinal Injuries Centre, Stoke Mandeville Hospital, Aylesbury, Bucks HP21 8AL, UK. METHODS: A total of 53 studies were carried out on 52 patients between 1962 and 1964. In all, 49 patients were studied during the first 10 days after injury as follows: a control group of 39 patients received no supplementary sodium, two received NaCl infusion, two NaCl tablets orally, and six received NaCl infusion followed by NaCl tablets orally. Four patients were studied for more than 15 days after injury (one of these had been studied in the acute stage); they received NaCl infusion and one (42d) received in addition NaCl tablets for four subsequent days. RESULTS: In all patients urinary sodium excretion was minimal on day 2 and increased thereafter. On days 2-6, it was significantly lower in patients with a complete transection of the cervical cord than in patients with lower lesions. In the early studies, nine patients excreted less than 40% of the administered load within 24 h. In four of these patients excretion was 10% or less. In the later studies, three of the four patients excreted at least 80% of the infused Na+ on the same day. CONCLUSION:Sodium retention in the patient with cord injury is a response to trauma. The different responses seen in patients with different levels of cord transection are not due to direct changes in the innervation of the kidney but to compensation for sympathetic insufficiency, blood pressure being maintained by the secretion of aldosterone, vasopressin and other hormones. The decreased urinary output seen acutely after cord transection is not due to renal failure and the patient's condition can be made dangerously worse by attempts to create a diuresis.