Severity of community acquired hypernatremia is an independent predictor of mortality: a matter of water balance and rate of correction

Excerpt

Sodium balance disorders are the most frequent alterations among electrolyte disturbances. The subject of the retrospective single center study by Jung et al. [1] refers to an important clinical problem, mainly related to altered water balance responsible for dysnatremia. The results of this study indicate that the presence of hypernatremia (classified into mild 148–150 mEq/L, moderate 151–154 mEq/L and severe >155 mEq/L) at the time of admission or developing during the hospital stay represents an independent risk factor for development of longer hospital stay or mortality. In particular, the Authors evaluate in their study, the data collected from patients presenting to an urban tertiary hospital emergency department (ED), or from outpatients clinics during a period of 3 years. They label such a condition: community-acquired hypernatremia (CAH). With this premise, they find a low percentage (0.2% of all the admissions) of patients admitted to the hospital with hypernatremia of any degree (mild, moderate or severe). There are several points that should be carefully considered for the interpretation of the results observed in this study, and that should be taken as fundamental in the approach to hypernatremic patients. First, the prevalence of hypernatremia is rather low in the population considered in the study. The mean age of the studied population was almost 63 years-old. In the literature, the prevalence of hypernatremia, considering patients admitted to the ED, is reported to be from 5 to 10 times [2‐4] up to 20 times [5]. In intensive care unit, several studies report an even higher prevalence of hypernatremia [6‐8]. In their discussion, Jung et al. indicate that one of the possible causes of the prevalence discrepancies, might be partly ascribed to the older age of people evaluated in the majority of data reported in literature. This difference in ages might produce the variances, because water loss responsible for hypernatremia commonly develops in elderly patients whose access to water is limited as well as is their sense of thirst. In a recent paper, in contrast, it is reported that hypernatremia was the fourth most frequent electrolyte disorders in patients presenting to an ED (mean prevalence 4.4%) with a higher rate of presentation in a younger population (5.6 versus 3.7%) than in those older than 65 years of age (in contrast with what is expected) [5]. But Jung et al. clearly stated the different nature of CAH patients including outclinic patients from those hospitalized in intensive care units. Differences are observed in the pathogenesis of CAH and hospital acquired hypernatremia [9]. In the majority of all hypernatremic cases, hypernatremia is a hospital acquired condition. CAH is almost always hypovolemic, whereas hypernatremia acquired in hospital is not often linked to hypovolemia, and even in some patients, is related to fluid overload. It is important to distinguish hypernatremia linked to water loss also called dehydration from hypovolemia, where both sodium and water are lost [10]. Hypernatremia is most often related to unreplaced water loss from the gastrointestinal tract (vomiting or osmotic diarrhea due to laxatives), from the skin (excess of sweat because of fever or high ambient temperature), or from the urine (diabetes insipidus or an osmotic diuresis due to glucosuria in uncontrolled diabetes mellitus or to an excess of loop diuretic therapy such as furosemide). Because hypernatremia (through increased plasma osmolality) stimulates thirst and therefore the increase in water intake, this ionic disorder commonly occurs when patients are unable to sense thirst or to have an altered response to thirst. [10, 11] (Table 1). Much less common is the hypernatremia due to administration of salt in excess of water: such a condition can happen because of an inadvertent intravenous administration of hypertonic saline or to an exaggerated salt ingestion [12]. From the results of the study by Jung et al., it is of interest that the duration of hospital stay is greater in patients (according to the plasma sodium concentration value at hospital admission or to the maximum value reached during hospitalization) with severe hypernatremia as compared to those with mild or moderate levels of circulating sodium. More important in the results, is that the mortality rate observed during the hospital stay in patients with moderate or severe hypernatremia is higher than that of subjects with milder levels of natremia. From the Kaplan–Meier curves, it is evident that most of the mortality related to both the initial sodium levels (where a trend is present), and to the maximum value of plasma sodium reached during hospital stay (highly significant) occur in the first period of follow-up (almost all of the mortality observed occurs in the first 60–90 days). To better understand the prognosis of these patients, three fundamental elements should be known and clearly recognised: the cause or causes of hypernatremia, its duration and the therapeutic approach to correct hypernatremia (speed of correction). The cause of hypernatremia is the starting point in the diagnosis and evaluation of hypernatremic patient together with the recognition of the duration of hypernatremia. When approaching a patient with hypernatremia, it is necessary to know if the hypernatremia is acute or chronic. Hypernatremia that is present for longer than 48 h is considered chronic: the majority of patients have chronic hypernatremia, even those with hyperosmolarity-related acute mental status change, in whom hypernatremia is discovered; acute hypernatremia (present for less than 48 h) is less common. The correction of hypernatremia requires the administration of dilute fluids to correct the water deficit and replace the ongoing water loss [13]. Particular attention must be paid to the rate of serum sodium correction with the objective in patients with chronic hypernatremia to lower sodium levels by a maximum 10 mEq/L in a 24 h period (less than 0.5 mEq/L/h is considered safe), whereas in those with acute hypernatremia the objective is to lower sodium levels by 1–2 mEq/L/h to restore normal levels in less than 24 h. Fundamental is the frequent remeasurement of serum sodium levels, and to alter the hypotonic fluid replacement regimen accordingly. An excessive rapid correction of sodium levels in a patient with chronic hypernatremia can lead to cerebral edema, but also the under treatment of acute hypernatremia can generate permanent neurologic damage. In summary, the approach of treatment of hypernatremia involves several fundamental steps, starting from the estimation of water deficit, followed by the establishment of a proper rate of correction, and calculation of fluid repletion strategy by monitoring serum sodium concentration, also estimating the ongoing water and electrolytes loss (e.g., potassium). As Jung et al. state in the limitations of the study, there is a fundamental element that is missing that is strongly related to the prognosis and the survival of patients, especially when mortality is concentrated in the short term period. This element is represented by the strategy of treatment and the speed of correction of hypernatremia. This is fundamental when you approach a patient with sodium disorders, both hypernatremia but also hyponatremia [14]. This information would have given more strength to the interpretation and comprehension of the results of this study. …