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.     

Effect of sivelestat sodium on acute lung injury after acute aortic dissection

Acute lung injury is a frequent and serious complication in patients with acute aortic dissection (AAD). Elevated neutrophil elastase has been reported to be one of the major determinants occurring in AAD. On admission, we administered sivelestat sodium hydrate, a neutrophil elastase inhibitor, to 11 patients with AAD who were medically treated to prevent lung injury. We compared their clinical course with that of 12 patients of control group in which sivelestat was not used prophylacticaly. Although there were 5 patients (42%) who suffered from respiratory failure and needed mechanical ventilation in the control group, no one needed intubation in the sivelestat group. Our study suggested that sivelestat sodium hydrate could be effective in preventing intubation due to respiratory failure. Further prospective study is necessary to evaluate prophylactic administration of sivelestat sodium hydrate in AAD.     

Congenital sodium diarrhea in a neonate presenting as acute renal failure

Congenital sodium diarrhea is a rare cause of secretory diarrhea due to a defect in the sodium/proton exchanger that results in decreased sodium absorption and increased excretion in stools. We report a pre-term baby boy with a birth weight of 1.4 kg who was referred because of rapidly rising serum urea and creatinine. The initially reported high urine output was later found to be severe watery diarrhea with severe oliguria and acute renal failure. Associated findings were normal anion gap metabolic acidosis with hyponatremia that required >50 mmol/kg of sodium per day for correction and about 300 ml/kg per day of replacement fluid to correct fluid and electrolyte abnormalities. The patient continues to do well 5 months after diagnosis.     

A case of acute pneumococcal meningitis treated with spinal drainage and vancomycin administration

A 25-year-old woman complaining of general fatigue, headache, high fever, and nuchal rigidity, was admitted. She was diagnosed as pneumococcal meningoencephalitis after the cell culture of cerebrospinal fluid (CSF). Despite the administration of vancomycin (VCM), she fell into a coma without amelioration of the symptom. VCM was replaced by pipellaciline because antibacterial sensitivity showed the pneumococci were sensitive to the penicillins. She remained unconscious showing progressive hydrocephalus after the open drainage operation. The lumbar drainage at the L 4-5 level and the intrathecal administration of VCM were performed to improve the mal-circulation of CSF. After the procedure, the cell count of CSF showed a significant decrease and her consciousness level was recovered gradually. The patients with pneumococcal meningitis may occasionally require the lumbar drainage with the intrathecal administration of appropriate antibiotics, in case they fail to show response to the conventional therapy.     

Molecular mechanisms of sodium transport inhibition in proximal tubule during acute hypertension

Acute hypertension provokes a rapid decrease in proximal tubule salt and water reabsorption that increases the levels of sodium chloride at the macula densa, the error signal to increase arteriolar resistance to autoregulate renal blood flow and glomerular filtration rate, and contributes to pressure natriuresis. The molecular mechanisms responsible for this critical homeostatic adjustment are beginning to be dissected: apical sodium transporters in the proximal tubule are redistributed out of the brush border to intermicrovillar and endosomal stores and sodium pump activity is inhibited. These responses are strikingly similar to the cellular responses to parathyroid hormone, and are mediated by similar signalling pathways.     

牛磺胆酸钠诱导的急性坏死性胰腺炎大鼠脏器功能障碍观察

目的 探讨急性坏死性胰腺炎大鼠脏器功能障碍及病程演进规律.方法 大鼠分为两组,急性坏死性胰腺炎(acute necrosis pancreatitis,ANP)组64只,对照组48只.采用经胰管逆行注射5%牛磺胆酸钠诱导ANP,对照组予胰管内注射生理盐水.分别于模型诱导后3、6、9、12、18、24 h(每一时间点各8只大鼠)处死,测定大鼠呼吸、体温、心率、血白细胞、肝肾功能及血气分析,另有16只ANP大鼠观察其24 h生存率.结果 ANP组24 h生存率为75%.ANP组在模型制备后3 h体温、心率、血白细胞明显高于对照组(P<0.05),6 h血清乳酸脱氢酶水平显著升高(2 613 vs 1822 IU/L.P<0.05),9 h血清肌酐水平显著升高(27.5vs 18.7 μmol/L,P<0.05),12 h动脉血PaO2显著降低(7.8vs 12.5 kPa,P<0.05),18 h之后各脏器处于衰竭期.对照组无脏器功能障碍表现.ANP组各时间点胰腺病理学评分显著高于对照组.结论 在5%牛磺胆酸钠诱导的ANP病程中,3 h后出现全身炎症反应综合征,6 h出现肝功能障碍,9 h后进入多脏器功能障碍期,18 h后进入多脏器衰竭期.     

Chloride levels in meningitis

The blood/cerebrospinal fluid bromide ratio is sensitive and specific in the diagnosis of tuberculous meningitis (TBM). Blood/CSF chloride (Cl-) ratios were not found to be useful in differentiating between TBM and viral and acute bacterial meningitis in 59 black children. In a study of 148 children with bacterial or viral meningitis or TBM, the majority (112) had CSF Cl- levels below the lower limit of normal. Accordingly, CSF and blood Cl- levels and the blood/CSF Cl- ratio were not found to be useful in differentiating between TBM, acute bacterial meningitis and viral meningitis.     

Post-traumatic meningitis in children

A retrospective survey over a 66-month period of children admitted with head injury who subsequently developed meningitis within the same period yielded six cases (five boys, one girl), giving an incidence of 0.38 per cent. Two of the six died, and four survived with no sequelae. Four cases occurred within the first week. One patient, who had received prophylactic antibiotics, developed Escherichia coli meningitis after 14 days and one had meningitis 2 years after the head injury. The most common organism was pneumococcus (four cases). Three patients had periorbital haematomas and none had cerebrospinal fluid leakage. Increasing drowsiness and fever were the most consistent features. Radiography of the skull was of little use in demonstrating fracture of the base of the skull. Two of the four surviving patients had craniotomy with successful dural repair.     

Tuberculous meningitis in children

Opinion statement  

Systemic inflammatory response syndrome and acute renal failure associated with Hemophilus influenzae septic meningitis

Sepsis is often associated with a downward spiral through a spectrum of systemic inflammatory response syndrome (SIRS) culminating in organ failure and death. Here we present a 3-year-old girl with Hemophilus influenzae septic meningitis who developed SIRS and acute renal failure. In the initial stage, the patient showed uremia, cytopenia, disseminated intravascular coagulation, elevation of tissue enzyme and ferritin values, hemophagocytosis and overproduction of nitric oxide. The serum cytokine profile revealed increased levels of soluble interleukin (IL)-2 receptor, IL-6, IL-10 and tumor necrosis factor alpha. The patient responded positively to early and intensive interventions including antibiotics, repeated exchange transfusions, dexamethasone and high-dose gamma-globulin. The above laboratory abnormalities almost normalized with clinical improvement. We consider that SIRS was probably responsible for the sequence of events resulting in renal failure in this case, and suggest that renal failure should be included among the serious complications of SIRS associated with Hemophilus influenzae septic meningitis.     

Bacterial meningitis

Opinion statement Initial empiric therapy for community-acquired bacterial meningitis should be based on the possibility that penicillin-resistant pneumococci may be the etiologic organisms and, hence, should include a combination of third-generation cephalosporin (cefotaxime or ceftriaxone) and vancomycin. Ampicillin should be included if the patient has predisposing factors that are associated with a risk for infection with Listeria monocytogenes. Bacterial isolates from the cerebrospinal fluid should be tested for antimicrobial susceptibility. Understanding the significance of inflammatory cytokines in the pathophysiology of bacterial meningitis leads to an understanding of the need to prevent their formation. Dexamethasone inhibits synthesis of the inflammatory cytokines, interleukin-1 and tumor necrosis factor. Results of clinical trials and meta-analysis suggest that dexamethasone therapy improves the outcome for patients with bacterial meningitis. Dexamethasone should be administered before or with the first dose of antibiotics. The development of therapeutic modalities to downregulate host inflammatory responses, such as those of monoclonal antibodies to cytokines, is of utmost importance.