Hyponatremia and Oxidative Stress

Hyponatremia, i.e. the presence of a serum sodium concentration ([Na+]) < 136 mEq/L, is the most frequent electrolyte imbalance in the elderly and in hospitalized patients. Symptoms of acute hyponatremia, whose main target is the central nervous system, are explained by the “osmotic theory” and the neuronal swelling secondary to decreased extracellular osmolality, which determines cerebral oedema. Following the description of neurological and systemic manifestations even in mild and chronic hyponatremia, in the last decade reduced extracellular [Na+] was associated with detrimental effects on cellular homeostasis independently of hypoosmolality. Most of these alterations appeared to be elicited by oxidative stress. In this review, we focus on the role of oxidative stress on both osmolality-dependent and -independent impairment of cell and tissue functions observed in hyponatremic conditions. Furthermore, basic and clinical research suggested that oxidative stress appears to be a common denominator of the degenerative processes related to aging, cancer progression, and hyponatremia. Of note, low [Na+] is able to exacerbate multiple manifestations of senescence and to decrease progression-free and overall survival in oncologic patients.

Acute Severe Hyponatremia following Hysteroscopic Procedure in a Young Patient: A Case Report and Review of the Literature

Background. Hysteroscopic surgery is a minimally invasive procedure used to diagnose and treat intrauterine pathologies. It requires distension of the uterine cavity for the adequate visualization of the operative field. Glycine (1.5%) is one of the most commonly used solutions because it is nonconductive and also has good optical properties. However, acute hyponatremia is a critical complication that can develop after the absorption of a sufficient amount of the irrigation medium. Case Presentation. We report a case of a 43-year-old female patient who developed acute symptomatic hyponatremia (104 mEq/L) and pulmonary edema secondary to hysteroscopic resection of leiomyoma and hastily approached with rapid sodium correction measures. Conclusion. Multiple strategies can be taken to reduce the risk of fluid absorption and subsequent hyponatremia. Moreover, attention should be paid to the treatment approach for patients with acute hyponatremia following hysteroscopic procedures; rapid correction of acute hyponatremia for such patients might be safe, although there is no consensus in the literature, and further trials are needed.

Acute and Chronic Hyponatremia

Hyponatremia is the most common electrolyte disorder in clinical practice. Catastrophic complications can occur from severe acute hyponatremia and from inappropriate management of acute and chronic hyponatremia. It is essential to define the hypotonic state associated with hyponatremia in order to plan therapy. Understanding cerebral defense mechanisms to hyponatremia are key factors to its manifestations and classification and subsequently to its management. Hypotonic hyponatremia is differentiated on the basis of urine osmolality, urine electrolytes and volume status and its treatment is decided based on chronicity and the presence or absence of central nervous (CNS) symptoms. Proper knowledge of sodium and water homeostasis is essential in individualizing therapeutic plans and avoid iatrogenic complications while managing this disorder.

Hyponatremia caused by water intoxication: successful treatment of psychiatric disturbances with olanzapine and fluoxetine

ABSTRACT Hyponatremia is a frequent, yet often unrecognized result of water intoxication caused by psychogenic polydipsia in patients with psychiatric disorders such as schizophrenia and anorexia nervosa. The consequences of hyponatremia may include cerebral edema with tonic–clonic seizures and, in extreme cases, death. In cases of hyponatremia seen in psychiatric practices, the use of psychotropic drugs is often necessary to address both the underlying psychiatric problem and reduce the hyponatremia. Therefore, a patient’s clinical condition, the risk of side effects, the possible effect of the medication on hyponatremia and a history of prior medication use should be considered when selecting appropriate psychotropics. The present clinical case details the beneficial effects of olanzapine and fluoxetine in treating a patient with anorexia nervosa and body dysmorphic disorder experiencing acute hyponatremia, and the stable effect the medications achieved over a period of 2.5 years of maintenance therapy.

Acute isotonic hyponatremia after single dose histidine-tryptophan-ketoglutarate cardioplegia: an observational study

Introduction: Histidine-tryptophan-ketoglutarate cardioplegia is used for prolonged myocardial protection in complex cardiac surgery. Administration leads to acute hyponatremia in a majority of patients, because of its low sodium concentration (15 mmol/L). However, histidine-tryptophan-ketoglutarate solution’s osmolality is slightly hypertonic (310 mOsm/kg). Hypothesized was that acute isotonic hyponatremia will be induced, which does not need to be corrected with hypertonic saline. Methods: Cardiac surgery patients who received histidine-tryptophan-ketoglutarate cardioplegia were included in this prospective single center study. Serial blood samples were taken from each patient at five different time points: after induction of anesthesia (T1) and 10 minutes (T2), 6 hours (T3), 12 hours (T4), and 18 hours (T5) after administration of histidine-tryptophan-ketoglutarate cardioplegia, respectively. Blood samples were analyzed for sodium concentration, osmolality, and acid-base balance. Results: Twenty-five patients were included. Median blood sodium levels decreased from 140 [138-141] at T1 to 128 [125-130] mmol/L at T2 (p < 0.001). At T3, T4, and T5, median blood sodium concentrations were 136 [134-138], 139 [137-140], and 140 [137-142] mmol/L, respectively. Median osmolality was 289 [286-293] at T1 and increased to 296 [291-299] mOsm/kg (p < 0.001) at T2. At T3, T4, and T5, osmolality was 298 [292-302], 298 [294-304], and 300 [297-306] mOsm/kg, respectively. Median pH decreased from 7.38 [7.36-7.40] at T1 to 7.30 [7.27-7.32] at T2 (p < 0.001). Conclusion: Administration of histidine-tryptophan-ketoglutarate cardioplegia during cardiac surgery leads to acute moderate to severe isotonic hyponatremia, which resolves spontaneously in the first 18 hours perioperatively. Correction with hypertonic saline is not necessary.

SUN-352 The Effects of Acute Hyponatremia on Bone Remodeling Markers in Patients with Subarachnoid Hemorrhage

Animal data and cross-sectional human studies have established that chronic hyponatremia predisposes to osteoporosis; the effects of acute hyponatremia on bone remodeling are unknown. Serum markers of bone remodeling (total procollagen type 1 amino-terminal propeptide (P1NP), bone specific alkaline phosphatase (bone ALP), N-mid-osteocalcin (OCI) and C-terminal teleopeptides of type I collagen (CTX-1)) were assessed in a cohort of patients admitted with subarachnoid hemorrhage (SAH), who were prospectively studied over seven days. The ratio of P1NP:CTX-1 was calculated to report a bone formation index. Twenty-two patients (13 women), median (IQR) age 53 (47, 62) years were recruited. Patients who developed post-SAH ACTH deficiency and those treated with glucocorticoids, or continuous enteral feeding were excluded. All patients were eunatremic on initial assessment. Eight patients developed acute hyponatremia, median nadir plasma sodium concentration (pNa) 131 (128, 132) mmol/L, and 14 remained eunatremic, nadir pNa 136 (133, 137) mmol/L. The groups were matched for age, 25-hydroxy Vitamin D, PTH, WFSS and Fischer scores. Serum cortisol concentration was greater in the hyponatremic group, 571 (504, 671) nmol/L, than the eunatremic group, 449 (400, 501) nmol/L, p=0.008. Bone remodeling markers and bone formation index (P1NP:CTX-1 ratio) were similar in the two groups at baseline. There was a significant rise in CTX-1 in both hyponatremic patients, +0.15 (0.09, 0.37) μg/l, p = 0.009, and patients who remained eunatremic, +0.11 (-0.02, 0.23) μg/l, p = 0.04, with no significant difference between the groups. There was, however, a significant fall in P1NP:CTX-1 ratio in patients with acute hyponatremia, p = 0.02, but no significant change in eunatraemic patients, with significant between group difference, p = 0.02. Changes in P1NP and OCI correlated positively with nadir pNa; r = 0.43, p = 0.04 and r = 0.61, p = 0.001 respectively. In addition, there was a positive correlation between change in P1NP:CTX-1 ratio and nadir pNa, r = 0.43, p = 0.04. There was no correlation between change in OCI or CTX-1 and nadir pNa. Serum cortisol was strongly negatively correlated with change in P1NP (r = -0.64, p = 0.001) but not with change in other bone remodeling markers. Acute hyponatremia following SAH is associated with a fall in bone formation index; physiological hypercortisolemia may contribute to this. Further analysis with larger numbers will help us determine whether hyponatremia is an independent risk factor.