| BackgroundThe normal range of blood natrium is 135-145mmol/L. Hypernatremia is when blood natrium is over 145mmol/L. It’s a kind of common electrolyte disturbance in ICU patients. According to domestic or oversea reports, the incidence of hypernatremia in ICU patients is about 2%-6%, whereas the incidence of iatrogenic hypernatremia is about 6%-24%. Hypernatremia can impact on several systems including neuromuscular, cardiovascular, digestive systems and etc. Among them, the impact on neural system is especially common and severe. In addition, treatment for hypernatemia in ICU patients is difficult and sometimes ineffective due to the complexity and severity of the patients’ condition. Thus hypernatremia is one of the risk factors to affect the patients’ prognosis. It has been reported that the mortality of severe hypernatremia patients is up to 30-50%. Similar with hypernatremia, sepsis, with feature of high incidence and high mortality, is a common disease in ICU. Sepsis is the systemic inflammatory response to microbial infection. According to oversea reports, in 1000 people,2.4 to 3 cases of sepsis occur. About 750000 cases of sepsis occur each year. Sepsis is one of the main reasons for death of critical patients, with a mortality of 14.7% to 29.9%. Thus it’s also an important target to focus on and a hot area of research in critical medicine.Critical patients often suffer in sedation or coma, unable to regulate electrolyte free water balance through thirst mechanism and turn into hypernatremia due to loss of too much electrolyte free water. Apart from this, pathological change induced by primary disease, inappropriate fluid management, and excessive injection of medicine with high concentration of sodium (e.g. sodium bicarbonate, voriconazole, hypertonic sodium chloride) are important reasons for elevation of blood natrium. As for this, some oversea scholars generalized the mechanism of hypernatremia into two points:loss of electrolyte free water or (and) excessive intake of hypertonic sodium-laden fluid. The existing reports about mechanism of hypernatremia are likely concentrated on relation between hypernatremia and primary disease, intake of sodium and etc., few of them directly study the relation between hypernatremia and sodium excretion.Pathways of sodium excretion include renal, gastrointestinal, dermal, respiratory ways and etc.90% of the sodium is excreted via kidney. Urine sodium is a decent indicator to measure sodium excretion from kidney. Most of the existing reports about hypernatremia mechanism are retrospective studies which are often lack of data related with urine sodium. Thus few studies about hypernatremia mechanism have been reported. Nevertheless, quite a few scholars believe that urinalysis, including urine sodium, urine potassium, urine creatinine analysis and etc., are essential instructions for abnormal blood natrium, especially for hypernatremia. Some scholars even suggest that patients with hypernatremia should perform urinalysis everyday. Although the collection of 24h urine sodium is more complicated than that of random urine sodium, it possesses a better reflection of 24h urine sodium excretion. So we chose 24h urine sodium as the indicator of urine sodium excretion. Clinical data of 200 cases and 572 days (one patient per day) of critical patients were collected in this study to explore the relation between urine sodium and blood sodium, further understand the role of abnormal sodium excretion in hypernatremia mechanism, so as to provide better treatment and prognosis for hypernatremia patients. Intention1. Discuss effect of urine sodium in the hypernatremia mechanism.2. Discuss relevant factors that induce urine sodium change, e.g. hormone aldosterone,, creatinine level.3. Discuss the relation between urine sodium and prognosis of critical patients.Method1. SubjectData from patients hospitalized between September,2013 to February,2015 were collected.200 cases (572 days) were available, including 153 male patients and 47 female patients. Average age was 53.7±23.4 years. Average APACHE II score was 24.5±9.6. There were 83 cases of sepsis,30 cases of trauma,34 cases of hypoxic-ischemic encephalopathy,29 cases of cerebrovascular accident,10 cases of heart failure,14 cases of gastrointestinal hemorrhage, diabetic ketoacidosis, terminal cancer and etc. Exclusion criteria:① Cases with blood purification treatment (including dialysis, continuous renal replacement therapy, plasma exchange and etc.) or bladder irrigation. Cases with hospitalization less than 1 day and alike situations (24h urine sodium cannot be obtained accurately in such cases). ②Cases with incomplete information. This study conforms to the standards of medical ethics and was approved by the Hospital Ethics Committee.2. Method2.1 Observation and RecordingCases that met the criteria were collected from the second day of hospitalization. Cases with hospital stay over 3 days were collected for 3 days. Cases with hospital stay less than 3 days were collected for the 1 or 2 days of their hospitalization. Data were recorded including age, gender, main diagnosis at admission, APACHE II scores, 28-day prognosis, daily input-output volume (input included gastrointestinal and intravenous input, output included urinary, gastric, rectal output and drainage), average daily blood sodium level, average daily lactic acid level, urine sodium concentration,24h urine sodium level, sodium input amont (intravenous and gastrointestinal input), serum creatinine level, morning decubital aldosterone level and antidiuretic hormone level.2.2 Some important data collecting method2.2.124h urine sodium concentration and level collecting and detecting methodAfter adding urine preservative methylbenzene 5-10ml into urine collector, collect the patient’s 24h urine. Mix the collected urine thoroughly and take appropriate amount to test urine sodium concentration. Multiply urine sodium concentration (mmol/L) by 24h urine volume (L) to produce 24h urine sodium level.2.2.2 Aldosterone testingDraw intravenous blood 2mL at morning decubitus and place it into anticoagulant tubes. Mix it completely and let stand for 1h. Then centrifuge it. Draw 1 mL supernatant into EP tube after centrifuge. Temporarily freeze it into -20℃ refrigerator. Limit freezing time in 90 days. Perform ELIS A in batch within a month.Testing method:Draw 0.05mL reference standards and samples into the tubes with quality control. Draw 0.1mL aldosterone markers and 0.1mL anti-aldosterone antiserum into the tubes respectively. After adding the reagents, cover plastic films on the tube rack and swing it softly on vortex mixer. After swing, incubate it in 37℃ water bath for 60min. Then add lmL fully mixed separating medium to the rest of tubes (apart from the main tube). Let stand for 10 min after fully mixed and swung. Centrifuge again for 15min. Sop up the supernatant and perform count for 1min.Connect to the software. It will load data from the counter automatically and draw standard curve based on the standard tube and’0’tube. Aldosterone concentration will be automatically calculated correspondingly.2.3 Grouping MethodAfter gathering all needed information, the cases were separate into 2 groups according to blood sodium level and urine sodium level: ①According to the patients’ daily blood sodium level,3 groups were generated as low blood sodium group (<135mmol/L), normal blood sodium group (135-145mmol/L) and high blood sodium group (>145mmol/L).②According to the patients’diagnosis at admission, patients were separated into sepsis group and no sepsis group. ③According to the patients’ 24h urine sodium level,3 groups were generated as low urine sodium group (<130mmol/d), normal urine sodium group (130-260mmol/d) and high urine sodium group (>260mmol/d).④According to the patients’ average urine sodium level during hospitalization,3 groups were generated as low urine sodium group (<130mmol/d), normal urine sodium group (130-260mmol/d) and high urine sodium group (>260mmol/d). Compare 28-day mortality among the groups.3. Statistical MethodAfter normal distribution test, measurement data that accorded with normal distribution were presented as mea±tSD (x±s). Means of three groups were compared using one-way ANOVA. Two groups were compared using Bonferroni or Dunnett-t. Data that didn’t accord with normal distribution were presented as median (interquartile rage) and compared with nonparametric test. Count data were tested using χ2 test. P<0.05 was considered as statistical significant.Result1. Compare of groups separated according to blood sodium level200 cases and 572 days (one patient per day) of data were collected. Data were categorized according to normal range of blood sodium level as below,402 days of hypematremia,132 days of normal blood sodium,38 days of hyponatremia. ① Compare hypernatremia group with normal blood sodium group:The blood glucose level, total input volume, lactate level, creatinine level and APACHE II score (at admission of ICU) of hypernatremia group were all higher than those of the normal blood sodium group (all P<0.05), whereas the urine sodium concentration and 24h urine sodium level were lower (both P<0.05). No significant difference of the total sodium input amont, urine volume, total output volume, aldosterone level was seen between these two groups (all P>0.05).②Compare hyponatremia group with normal blood sodium group:The urine sodium concentration,24h urine sodium level, sodium input amount of hyponatremia group were all higher than those of normal blood sodium group (all P<0.05), whereas the ceatinine level was lower (P<0.05). No significant difference of blood glucose level, lactate level, APACHE II score, urine volume, total output volume and aldosterone level was seen between these two groups (all P>0.05).2. Comparison between sepsis group and no sepsis group200 cases of patients were collected, among them were 83 cases with sepsis and 117 cases without sepsis. Blood sodium level, lactate level and sodium intake volume of septic patients were all higher than the non-septic patients (P<0.05), whereas no statistical difference was found of creatinine level,24h urine sodium level and urine sodium concentration between them (all P>0.05).3. Compare of groups separated according to urine sodium levelData were categorized according to the normal range of urine sodium level as below,259 days of low urine sodium,213 days of normal urine sodium,100 days of high urine sodium. ①Compare the low urine sodium group with normal urine sodium group:The APACHE Ⅱ score, blood sodium level, creatinine level, lactate level, aldosterone level of low urine sodium group were all higher than those of normal urine sodium group (all P<0.01), whereas the urine volume, total output volume were lower (both P<0.01). No significant difference of total input volume, sodium input amount and blood glucose level was seen between these two groups (all P>0.05). ②Compare high urine sodium group with normal urine sodium group:The sodium input amount, total input volume, urine volume, total output volume of the high urine sodium group were all higher than those of the normal urine sodium group (all P<0.01). Whereas no significant difference of the APACHE II score, aldosterone level, blood sodium level, lactate level, blood glucose level and creatinine level was seen between these two groups (P>0.05).4. Urine Sodium and PrognosisDefine one patient as one case. Categorize data according to the average 24h urine sodium level during hospitalization in ICU.200 cases were collected, among them were 101 cases in low urine sodium group,62 cases in normal urine sodiumgroup and 37 cases in high urine sodium group. Low urine sodium group contained 68 cases of death and with a 28-day mortality of 67.3%. Normal urine sodium group contained 12 cases of death, with a 28-day mortality of 19.4%. High urine sodium group contained 10 cases of death, with a 28-day mortality of 27.0%. A statistical difference of mortality was seen among these three groups. Pairwise comparison result:Mortality of low urine sodium group was higher than the normal urine sodium group (P<0.0001). No significant difference of mortality was seen between the high urine sodium group and the normal urine sodium group (P=0.455). Mortality of the low urine sodium group was higher than the high urine sodium group (P<0.0001).Conclusion1.Reduction of natriuresis is a significant reason for hypernatremia.2.Reduction of natriuresis may relate with decline of kidney function, abnormal concentration of hormone or insufficient circulating blood volume and etc.3.Prognosis of critical patients with reduction of natriuresis is dismal, with a relatively high 28-day mortality. |
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