Elderly with refractory chronic severe hyponatremia and anesthesia management dilemma: a case report with literature review

Hyponatremia is a common electrolyte disorder, especially in the frail elderly population. With the increasing number of surgeries in the aging population, hyponatremia is frequently encountered by anesthesiologists and surgeons. Unfortunately, management of hyponatremia is often complex in the elderly population as it is often multifactorial, and they are physiologically susceptible. While it is well known that preoperative hyponatremia is associated with increased perioperative morbidity and mortality, a lack of recommendations or guidelines adds to the dilemma in managing such cases. The most common cause of chronic hyponatremia in the elderly is the syndrome of inappropriate antidiuretic hormone (SIADH), which can be resistant to conventional treatment. On the other hand, paraneoplastic SIADH leading to hyponatremia is rare, and surgery may be the only option available for its correction. We present a case of a 78- years-gentleman to highlight such a dilemma. He was diagnosed with renal cell carcinoma and had chronic refractory severe hyponatremia despite treatment with fluid restriction, low dose hydrocortisone, tolvaptan, and 3% sodium chloride.

Influence of Hyponatremia on Spinal Bone Quality and Fractures Due to Low-Energy Trauma

Background and Objectives: Hyponatremia is the most common electrolyte disorder in elderly and associated with increased risk of falls. Clinical studies as well as small animal experiments suggested an association between chronic hyponatremia and osteoporosis. Furthermore, it has been assumed that subtle hyponatremia may be an independent fracture risk in the elderly. Therefore, this study was designed to evaluate the possible influence of chronic hyponatremia on osteoporosis and low-energy fractures of the spine. Materials and Methods: 144 patients with a vertebral body fracture (mean age: 69.15 ± 16.08; 73 females and 71 males) due to low-energy trauma were treated in a level one trauma center within one year and were included in the study. Chronic hyponatremia was defined as serum sodium < 135 mmol/L at admission. Bone mineral density (BMD) of the spine was measured using quantitative computed tomography in each patient. Results: Overall, 19.44% (n = 28) of patients in the low-energy trauma group had hyponatremia. In the group with fractures caused by low-energy trauma, the proportion of hyponatremia of patients older than 65 years was significantly increased as compared to younger patients (p** = 0.0016). Furthermore, there was no significant gender difference in the hyponatremia group. Of 28 patients with chronic hyponatremia, all patients had decreased bone quality. Four patients showed osteopenia and the other 24 patients even showed osteoporosis. In the low-energy trauma group, the BMD correlated significantly with serum sodium (r = 0.396; p*** < 0.001). Conclusions: The results suggest that chronic hyponatremia affects bone quality. Patients with chronic hyponatremia have an increased prevalence of fractures after low-energy trauma due to a decreased bone quality. Therefore, physicians from different specialties should focus on the treatment of chronic hyponatremia to reduce the fracture rate after low-energy trauma, particularly with elderly patients.

Low Creatininuria due to Hyponatremia Is Reversible in Many Patients

<b><i>Background:</i></b> Chronic hyponatremia has been reported to be associated with low solute intake and low creatinine excretion (reflecting likely sarcopenia). We wanted to study the effect, on the long term, of correction of hyponatremia on solute and creatinine excretion in chronic SIADH. <b><i>Methods:</i></b> We made a retrospective review of clinical and biochemical data of patients with euvolemic hyponatremia. We analyzed 24-h urine solute and creatinine excretion in volunteers with hyponatremia induced by dDAVP over 4 days, in 12 patients with chronic SIADH (&#x3e;1 month) before and after a few days of SNa correction and in 12 patients (6 women and 6 men) before and after 3 months of SNa correction by a vaptan or urea. <b><i>Results:</i></b> We confirm a low urine creatinine and solute excretion only in patients with chronic hyponatremia (&#x3e;1 month). Correction of SNa (from 127 ± 2.3 mEq/L to 139 ± 2.8 mEq/L) for &#x3e;3 months, in the 12 patients (mean age 58 ± 18), was associated with an increase in 24-h creatinine excretion (from 986 ± 239 to 1,238 ± 220 mg; <i>p</i> &#x3c; 0.02) and in patients treated with a vaptan (<i>n</i> = 5) solute excretion increased from 656 ± 207 mmol/24 h to 960 ± 193 mmol/24 h (<i>p</i> &#x3c; 0.02). Sodium excretion increased also in the 12 patients (from 100 ± 53 mEq/24 h to 169 ± 38 mEq/24 h; <i>p</i> &#x3c; 0.01). <b><i>Conclusion:</i></b> Chronic hyponatremia (&#x3e;1 month) is associated with a decrease in solute output (or intake) and in creatinine excretion. In many patients, these abnormalities are reversible in the long term.

Hyponatremia Intervention Trial (HIT): Study Protocol of a Randomized, Controlled, Parallel-Group Trial With Blinded Outcome Assessment

Background: Hyponatremia is the most common electrolyte disorder with a prevalence of up to 30% in hospitalized patients. In contrast to acute hyponatremia where the need for immediate treatment is well-recognized, chronic hyponatremia is often considered not clinically relevant. This is illustrated by reports showing that appropriate laboratory tests are ordered in &lt;50% of patients and that up to 75% are still hyponatremic at discharge. At the same time, emerging evidence suggests an association between hyponatremia and adverse events including increased risk of mortality and rehospitalization.Methods: This is a randomized (1:1 ratio) controlled, superiority, parallel-group international multi-center trial with blinded outcome assessment. In total 2,278 participants will be enrolled. Participants will be randomly assigned to undergo either targeted correction of plasma sodium levels or standard of care during hospitalization. The primary outcome is the combined risk of death or re-hospitalization within 30 days.Discussion: All data on hyponatremia and mortality are derived from observational studies and often lack methodologic robustness. Consequently, the direct impact of hyponatremia on mortality and rehospitalization risk is still debated, resulting in a clinical equipoise whether in-hospital chronic hyponatremia should be treated or not. Therefore, a randomized controlled trial is required to study whether targeted plasma sodium correction reduces the risk of mortality and rehospitalization associated with hyponatremia.Clinical Trial Registration:www.ClinicalTrials.gov, identifier: NCT03557957.

Chronic hyponatremia based on maxillary sinus mass

Summary This is a case report of a child with chronic hyponatremia due to the syndrome of inappropriate antidiuretic hormone secretion (SIADH) as a paraneoplastic manifestation of olfactory neuroblastoma (OFN). We hereby report a clinical presentation as well as a pragmatic approach to one of the most common electrolytic disorders in the pediatric population and have emphasized the necessity of involving the sinonasal area in the diagnostic procedure while evaluating possible causes of SIADH. This report indicates that the chronicity of the process along with the gradual onset of hyponatremia occurrence is responsible for the lack of neurological symptoms at the moment of disease presentation. Learning points Hyponatremia is not infrequently attributed to SIADH. Paraneoplastic syndromes are uncommon but they should be considered in the differential diagnosis of pediatric SIADH. Chronic insidious hyponatremia may not be associated with clear neurological symptoms despite its severity.

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.

Osmotic Demyelination Syndrome Following Correction of Hyponatremia by ≤10 mEq/L per day

Background: Overly rapid correction of chronic hyponatremia may lead to osmotic demyelination syndrome. European guidelines recommend a correction to ≤10 mEq/L in 24 hours to prevent this complication. However, osmotic demyelination syndrome may occur despite adherence to these guidelines. Methods: We searched the literature for reports of osmotic demyelination syndrome with rates of correction of hyponatremia <10 mEq/L in 24 hours. The reports were reviewed to identify specific risk factors for this complication. Results: We identified 19 publications with a total of 21 patients that were included in our analysis. The mean age was 52 years of which 67% were male. All of the patients had community acquired chronic hyponatremia. Twelve patients had an initial serum sodium <115 mEq/L, of which seven had an initial serum sodium ≤105 mEq/L. Other risk factors identified included alcohol use disorder (n=11), hypokalemia (n=5), liver disease (n=6), and malnutrition (n=11). The maximum rate of correction in patients with serum sodium <115 mEq/L was at least 8 mEq/L in all but 1 patient. In contrast, correction was <8 mEq/L in all but 2 patients with serum sodium >115 mEq/L. Among the latter group, osmotic demyelination syndrome developed before hospital admission or was unrelated to hyponatremia overcorrection. Four patients died (19%), 5 had full recovery (24%) and 9 (42%) had varying degrees of residual neurological deficits. Conclusions: Osmotic demyelination syndrome can occur in patients with chronic hyponatremia with a serum sodium <115 mEq/L despite rates of serum sodium correction <10 mEq/L in 24 hours. In patients with severe hyponatremia and high risk features, especially those with serum sodium <115 mEq/L, we recommend limiting serum sodium correction to <8 mEq/L. Thiamine supplementation is advisable for any hyponatremic patient whose dietary intake has been poor.

Longitudinal Study of Prevalence of Sodium Abnormalities in Hospitalized Patients With COVID-19

Background: Sodium abnormalities (dysnatremia) are frequently observed in patients with community-acquired pneumonia and are associated with excess mortality. Data on the prevalence of hyponatremia and hypernatremia (serum sodium [Na] &lt; 135 and &gt; 145 mmol/L respectively) in patients with coronavirus disease 19 (COVID-19) are currently lacking. Methods: The aim of this study was to evaluate the prevalence and etiology of hyponatremia and hypernatremia at several timepoints during hospitalization of COVID-19 patients. This retrospective, longitudinal, observational study included all COVID-19 positive adult patients admitted to two London hospitals over an 8-week period (February to May 2020). Results: Clinic records were reviewed in 488 patients, 277 males (56.8%) and 211 females (43.2%), with a median age of 68 years. Comorbidities were documented in 79.6%, with the commonest being hypertension (45.7%), diabetes mellitus (25%), and chronic kidney disease (16.4%). Prior to admission, 25 patients (5.1%) had pre-existing chronic hyponatremia. At hospital presentation, median [Na] concentration was 137 mmol/L. Dysnatremia was present in 146 patients (29.9%), including 26 (5.3%) with hypernatremia and 120 (24.6%) with hyponatremia, of whom [Na] was 130-134 mmol/L in 90 (18.4%) and &lt; 130 mmol/L in 30 (6.2%). Only 19% of patients with &lt; 130 mmol/L underwent adequate laboratory assessment of the etiology of hyponatremia. Of those, based on a urinary sodium cut-off of 30 mmol/L, hyponatremia was classified as hypovolemia in 75% and non-hypovolemic in 25%. For the remaining hyponatremic cases, using 5 mmol/L as the cut-off value for plasma urea, 55.7% were classified as probable hypovolemic and 44.3% non-hypovolemic hyponatremia. There was an upward trajectory of [Na] values during hospital stay with a median increase of 2 mmol/L in the first 48 hours following admission. On the fifth day of hospitalization, the prevalence was similar for hypernatremia and hyponatremia (13.8% and 14.1%, respectively). On the tenth day, hypernatremia was more common than hyponatremia (14.2% vs 10.2% respectively). Analysis of [Na] throughout the hospital stay defined four subgroups; 185 patients (37.9%) remained normonatremic throughout hospitalization; 180 (36.9%) had exposure to hyponatremia; 53 (10.9%) were exposed to hypernatremia; and 70 (14.3%) experienced both hypernatremia and hyponatremia. Conclusions: Hyponatremia, usually mild, was common at admission in Covid-19 positive patients, while hypovolemic hyponatremia appeared to be the predominant etiology. During hospital stay, abnormal sodium concentration was recorded in more than two thirds of Covid-19 positive patients. The association of dysnatremia with the outcomes in hospitalized COVID-19 patients warrants further exploration.

Challenges of Managing and Diagnosing Reset Osmostat vs SIADH in a Patient With Personal and Family History of Chronic Hyponatremia

Background: Distinguishing between a reset osmostat and SIADH in a hyponatremic patient can prove to be challenging in certain circumstances. Reset osmostat is an uncommon and under recognized cause of hyponatremia. Thus, it is important to recognize it as it does not require any treatment. Clinical Case: A 48 year old male with history of chronic hyponatremia of unknown cause, fatty liver, hypertension, was in the hospital post operatively after resection of a meningioma along dura. Endocrine was consulted for management of his chronic hyponatremia. Had chronic hyponatremia for over 20 years and was always asymptomatic. Normally drank 6-7 L of water at home, mostly at night. Also found to have a spinal compression fracture of unknown cause. Both his father and brother had chronic hyponatremia of unknown cause as well, suggesting possible familial component. His baseline sodium levels were 129-133 mmol/L. In the hospital, serum sodium levels decreased to the 120s. TSH was 0.307mcunit/mL (0.27-4.2). Was also placed on 1.5 L fluid restriction. Urine osmolality was 900 mOsm/kg (500-800) with sodium of 123 mmol/L (136-145), consistent with SIADH. A rare inherited disorder, nephrogenic SIADH (NSIADH), was considered. However, it has an X-linked inheritance pattern. Fluid restriction was removed, then did fluid load with 2L of water and obtained urine sodium, serum sodium, urine osmolality, serum osmolality, Copeptin (pro-AVP) before fluid load and 1 hour after fluid load. Serum sodium level went from 127mmol/L before to 125 mmol/L after. Urine osmolality improved from 984 mOsm/kg prior to 575 mOsm/kg after. Urine sodium went from 183 mmol/L prior to 91 mmol/L after. Serum osmolality went from 278 mOsm/kg (270-310) to 268 mOsm/kg after. His co-peptin pro-AVP levels were 16.4 pmol/L (ref. &lt;13.1). They are found to be low in NSIADH. It was decided that his chronic hyponatremia was likely due to reset osmostat. After discharge and follow up, his serum sodium was rechecked and was 128 mmol/L. It would have been challenging, but useful, to try a vaptan for diagnostic purposes and possibly to increase serum sodium. However, there are complications from overcorrection. Since patient had long standing asymptomatic chronic hyponatremia with family history, it was decided not to pursue aggressive measures just to “normalize” serum sodium. Otherwise, it would have been an example of treating the numbers and not the patient. Conclusions: Case demonstrates the importance of keeping the patient, their symptoms, and clinical picture in mind, and to not just follow numbers, as difficult as it may be, especially when managing conditions in which diagnosis may be uncertain or unclear. Sometimes no intervention is needed at all, however tempting it may be to do one, it is important to keep the former option in mind. An asymptomatic patient with longstanding chronic hyponatremia due to reset osmostat is an example of that.

Hyponatremia and Acute Kidney Injury as a Consequence of Malnutrition: A Case Report

This case presents how malnutrition due to underlying psychiatric disease can cause severe, chronic hyponatremia and acute kidney injury. A 31-year-old man was admitted due to fatigue. Blood tests displayed hyponatremia of 101 mmol/L and acute kidney injury. The patient had restricted himself to a uniform diet mainly consisting of rice boiled without salt. Isotone and hypertonic sodium chloride were used to secure a controlled rise in the sodium level. Despite fluid therapy, a delayed response in improvement in renal function was seen. After discharge, the patient started a balanced diet and the sodium level was almost normalized. Renal function eventually recovered. Long-term malnutrition may affect the tubular function of the kidney. Severe hyponatremia, other electrolyte disturbances, and protein and vitamin deficiency can be factors that interact in this pathogenesis. Resuming a normal diet may allow the kidney’s function to return to normal despite malnutrition during months.