Reduced sodium output following acute spinal injury.

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.

The reduced urinary output after spinal cord injury: a review.

Oliguria in patients following spinal cord injury was first mentioned in 1649, but has since been referred to only occasionally. The work detailed here was completed 30 years ago but is reported because of the lack of any comparable study and because suitable patients are not now readily available. A total of 27 water load tests were carried out on 20 patients. The test included measurement of serum osmolality to confirm absorption of ingested water. Impaired response to the water load was obtained in 17 tests: 12/13 between 1 and 5 days after onset of the cord lesion and 5/14 more than 2 weeks after injury. The possibilities that oliguria was due to dehydration, failure to absorb ingested water, hypotension or renal failure are discounted. In the first few days after injury, oliguria may be due to release of antidiuretic hormone as part of the metabolic response to trauma. The impaired response seen later is discussed in relation to possible neural and hormonal mechanisms. There is a need for further study of factors influencing water excretion in tetraplegic and paraplegic patients.

Liver enzyme studies with continuous intravenous anaesthesia.

A battery of liver function tests was carried out before operation and on the 3rd--5th and 13th--15th postoperative days in patients anaesthetised with continuous infusion of thiopentone, Althesin or etomidate for an intermediate operation. Some derangement of enzyme activity was found in one quarter to one third of the patients, and was most marked after Althesin. The findings are compared with published data on ketamine, which had an effect on enzyme activities similar to that of Althesin. On pooling data from different studies it became very apparent that large doses of intravenous anaesthetics cause a greater derangement of liver function than that which occurs using a balanced technique for the same operation.

Methodology of a prospective study of changes in liver enzyme concentrations following repeat anaesthetics.

The methodology of a large prospective study on the influence of repeated anaesthetics on liver function is reported and the problems involved are discussed. The most suitable patients were those presenting for endoscopic examination of the bladder and urethra, for urethral dilatation and for cervical implantation of radium. Blood samples were taken immediately before induction of anaesthesia and on days 3-4 and 13-15 after operation, when a clinical assessment of the patient was also carried out. The concentrations of six enzymes (lactate dehydrogenase, alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, serum cholinesterase and gamma glutamyl transpeptidase) werechosen specifically as indices of liver function. The eosinophil count was measured to reflect any hypersensitivity reaction. The non-Gaussian distribution of these necessitated using appropriate non-parametric tests together with parametric tests on logarithmic transformed data. In addition a quantal method was used to measure the frequency of patients showing an "abnormal" increase in enzyme concentrations.

A prospective study of liver enzyme and other changes following repeat administration of halothane and enflurane.

A prospective study of liver enzymes and other measurements following repeat administrations of halothane or enflurane was carried out in patients undergoing minor urological operations. The patient populations were similar with respect to frequency of factors which might influence liver function, social habits, drug therapy and time intervals between administrations. Sixty-three received two or more administrations of halothane and 66 received two or more administrations of enflurane, both drugs given with nitrous oxide in oxygen. There was a greater frequency of increased enzymatic activity following repeat administrations of halothane than following enflurane and the average alanine aminotransferase and gamma glutamyl transpeptidase concentrations were increased to a greater degree following halothane than enflurane. There was no change in the eosinophil count and no significant postoperative morbidity. Change in alanine aminotransferase, lactate dehydrogenase and gamma glutamyl transpeptidase occured more frequently in obese patients receiving halothane.

Changes in liver function after different types of surgery.

Liver function tests carried out after minor surgical procedures, under anaesthesia lasting for 1 hr, showed no abnormalities. Tests after body surface operations under the same anaesthetic techniques showed transient derangements. After intra-abdominal procedures, liver dysfunction was more marked, although no patients with evidence of preoperative liver dysfunction or postoperative surgical complications were studied and none received blood transfusions. Measurements of the serum bilirubin concentration showed the most frequent abnormalities, but the pseudocholinesterase concentration decreased progressively after intra-abdominal surgery and b.s.p. retention increased significantly. Serum concentration of intracellular enzymes (LDH, s.g.o.t. and s.g.p.t.) increased within an hour of starting surgery, changes which were probably not related to liver function.

The source of increased plasma potassium following succinylcholine.

Increases in plasma potassium following succinylcholine have been reported by many workers. In the present studies, these are greater when Althesin is used as the induction agent than after thiopental, and the rise is particularly marked in patients given halothane, occurring earlier in patients having electroshock therapy, and being reduced by the prior administration of a small dose of tubocurarine. These findings suggest that the rise in potassium is due to muscle trauma indiced by the relaxant during the period of fasciculation, and this is confirmed by an increase in creatine phosphokinase enzyme activity. Althesin and halothane are best avoided with succinylcholine in chronic catabolic states where an excessive rise in plasma potassium could lead to dangerous cardiac dysrhythmias.