
The prevalence and relevant factors of hyponatremia under long‐term total enteral nutrition: A cross‐sectional study
Author(s) -
Kajihara Yusaku
Publication year - 2017
Publication title -
journal of general and family medicine
Language(s) - English
Resource type - Journals
ISSN - 2189-7948
DOI - 10.1002/jgf2.44
Subject(s) - medicine , hyponatremia , gastroenterology , hypernatremia , hypokalemia , creatinine , anesthesia , sodium , chemistry , organic chemistry
Enteral nutrients contain the amounts of sodium (Na) above the estimated requirements (600 mg/d in Japan); however, some patients receiving enteral nutrition suffer from hyponatremia (HN) [serum Na level <135 mEq/L]. HN is the most common electrolyte disorder,1 and is associated with an increased risk of death in both an ambulatory setting and hospitalization even though the severity is mild.2,3 My retrospective study included 175 patients who had received a periodic replacement of gastrostomy catheters between April 1, 2012, and April 30, 2015, and who had been receiving total enteral nutrition for more than 5 months. There were no instances of fever, hypoxemia, vomiting, diarrhea, nephrotic syndrome, liver cirrhosis, or hemorrhagic diseases. The prevalence of HN was investigated and divided into three categories: mild [131—134 mEq/L], moderate [126—130 mEq/L], and severe [≤125 mEq/L]. Furthermore, I analyzed 128 patients, for whom no data were missing, to distinguish a difference between nonHN (n=68) and HN (n=60) groups in a number of wellknown associated factors: age, the period after gastrostomy, past history of cerebrovascular diseases (cerebral infarction, cerebral hemorrhage, subarachnoidal hemorrhage, or subdural hemorrhage), daily dosage of Na<600 mg/d, causative medications such as loop diuretics, thiazide diuretics, aldosterone antagonists, angiotensinconverting enzyme inhibitors, angiotensin II receptor blockers, nonsteroidal antiinflammatory drugs, or anticonvulsants (valproic acids, carbamazepine, or phenobarbital), serum total protein level, plasma glucose level, serum creatinine level, blood brain natriuretic peptide level, serum potassium level, and malignancies. I also used logistic regression modeling to examine the association between HN and potentially relevant factors,4 and sequentially introduced six variables including serum uric acid (UA) level, hemoglobin level, gender, serum albumin level, serum Creactive protein level, and medications for hyperuricemia into the model. All statistical analyses were conducted using EZR (Easy R) version 1.27, and a P value of <.01 was considered to be statistically significant. I used the twosided MannWhitney U test for the difference between two groups, and the Fisher’s exact test for the twobytwo frequency table. This study was approved by the Institutional Ethics Committee, and informed consent was obtained from the patients or their families. Seventythree patients (42%) had HN, but only five patients (3%) had severe HN (Table 1). There were no differences between two groups in the abovementioned associated factors. The adjusted odds ratio of the serum UA level was 0.59 per 1 mg/dL increment (99% confidence interval, 0.43—0.81). My study clearly demonstrates that HN is a common comorbidity under longterm total enteral nutrition and suggests the importance of monitoring serum Na level, although most cases of HN are mild or moderate. Additionally, it was revealed that serum UA level was significantly lower in the HN group. This study has two limitations. First, because the study design was a crosssectional, the causation of HN was unclear. Second, urine and endocrinological tests were not examined. Further studies are needed to investigate the relationship of a low serum UA level on the syndrome of inappropriate secretion of antidiuretic hormone.5 TABLE 1 The patients’ backgrounds (n=175)