Cause Of Hyponatremia Research Articles

Deciphering Familiar Conundrum of Cerebral Salt Wasting Syndrome vs Syndrome of Inappropriate Secretion of Antidiuretic Hormone and Establishing Role of Hyponatremia in Patients of Tuberculous Meningitis as a Predictor of Outcome.

Introduction: Hyponatremia is one of the most common electrolyte abnormalities [35-71%] associated with tuberculous meningitis [TBM]. It is an independent predictor of patient outcome. Cerebral salt wasting syndrome [CSWS] and syndrome of inappropriate secretion of antidiuretic hormones [SIADH] are two common causes of hyponatremia in patients with TBM. This study targets patients with tuberculous meningitis to provide a detailed analysis of hyponatremia in TBM patients and it’s predictive value in terms of outcome and also describes the distinguishing features of CSWS and SIADH. Materials and methods: This was a clinical, prospective study of 31 patients with TBM in which various parameters were analysed . Serial sodium levels were recorded on the day of admission, day 2, 7 and 28. Patients with hyponatremia were divided into CSWS and SIADH. Results: In this study, 24[77.42%] patients had hyponatremia. In 14 [58%], hyponatremia was due to CSWS and in 10[42%] of the patients with hyponatremia it was SIADH. Hyponatremia was related to disease severity, GCS score, hospital stay, ventilator stay and patient outcome. CSWS was more strongly associated with disease severity than SIADH. Conclusion: Hyponatremia is a common electrolyte imbalance in patients with TBM and a direct and valid predictor of disease outcome. CSWS should be differentiated from SIADH due to the different treatment strategies.

Syndrome of inappropriate antidiuresis/hyponatremia in COVID-19.

Hyponatremia is the most frequent electrolyte alteration among hospitalized patients and it has been reported in 20-40% of patients with SARS-CoV-2 (COVID-19) infection. Multiple causes of hyponatremia have been hypothesized in these patients. The syndrome of inappropriate antidiuresis (SIAD) has been considered one of the main reasons leading to hyponatremia in this condition. SIAD can be secondary to cytokines release, in particular IL-6. Positive pressure ventilation can be another cause of hyponatremia due to SIAD. Other possible etiologies of hyponatremia in COVID-19 patients can be related to secondary hypocortisolism, nausea, vomiting, heart and kidney damage. Similar to many other clinical conditions, there is strong evidence that hyponatremia is associated with a worse prognosis also in patients with COVID-19 infection. In particular, hyponatremia has been identified as an independent risk of ICU transfer, need of non-invasive ventilation and death. Hyponatremia in COVID-19 patients is in principle acute and symptomatic and should be treated as such, according to the published guidelines. Therefore, patients should be initially treated with i.v. hypertonic saline (3% NaCl) infusion and serum [Na+] should be frequently monitored, in order to remain within a safe rate of correction. There is evidence showing that serum [Na+] correction is associated with a better outcome in different pathologies, including COVID-19 infection.

Hyponatremia in geriatric patients.

Hyponatremia is the most frequent electrolyte imbalance in geriatric medicine. Causes of hyponatremia were retrospectively analyzed in all in-patients treated in 2016 (N = 2267, 1564 women, 703 men, mean age± standard deviation 81.9 ± 7.6years). Any form of hyponatremia on admission, during the stay or on discharge was noted in 308 patients (13.6%, 231 women, 77men; mean age± standard deviation 83.1 ± 7.3 years, p = 0.009 vs. age of all patients). Women had ahigher probability of developing hyponatremia compared to men (p = 0.019), 131 patients were hypovolemic, and dyspnea as an indicator of hypervolemia was noted in 71patients.Only 12patients suffering from hyponatremia (3.9%) did not receive any of the potentially sodium-lowering drugs assessed (diuretics, angiotensin-converting enzyme inhibitors, angiotensinII receptor antagonists, antidepressants, neuroleptics, nonsteroidal antirheumatics, carbamazepine, oxcarbazepine). The median number of drugs per patient potentially lowering the plasma sodium level was3 and the maximum number was7.Hypovolemic hyponatremia and the syndrome of inadequate antidiuretic hormone secretion were the most important causes of hyponatremia. Adverse drug effects were the main origins of both conditions. In patients with hyponatremia the drug load influencing plasma sodium level should be minimized, thiazide diuretics should be avoided and older individuals should receive adiet with sufficient salt content.

#1925 A rare cause of hyponatremia due to adrenal insufficiency in a patient with small cell lung cancer

Abstract Background and Aims Hyponatremia is the most frequent electrolyte disorder. Small Cell Lung Cancer (SCLC) release often antidiuretic hormone paraneoplastically. But Adrenal insufficiency is a rare cause of hyponatremia in SCLC. Prior one can cause euvolemic hyponatremia, latter one can cause hypovolemic hyponatremia. Opposite treatments should be applied for each one. So They should be investigated carefully before starting the treatment. Method A male patient who had metastatic SCLC was admitted to the emergency. After physical examination blood and urine tests were provided. Results A 52-year-old male patient who had metastatic SCLC was admitted to the emergency unit because of fatigue, weakness and confusion. On physical examination the patient's face was darkened but his conjunctiva was pale, his tongue and mucous membranes were dry. The blood pressure was 90/60 mm Hg. The test results provided were as follows: Glucose 106 mg/dL, creatinine 0.42 mg/dL, urea 38.1 mg/dL, sodium 109 mmol/L, potassium 3.3 mmol/L, white blood cells 9760 /mm3, hemoglobin: 9 g/dL, platelets: 176000/mm3. The patient had no chemotherapy during the last three months. He also did not have a history of antihypertensive treatment. The echocardiographic examination revealed that the ejection fraction was 60%. The abdominal computerized tomography scan showed multiple metastasis of the tumor, but adrenal glands were free of metastasis. The sodium deficit was calculated targeting to 120 mmol/L and therapy was started. The patient's weight was 70 kg. The calculated sodium deficit was 420 mmol. Since the hyponatremia was chronic, the deficit was planned to be given in 24 hours. Potassium was also given. During hospitalization, on day 2nd the patient's blood and urine tests were as follows: Creatinine 0.58 mg/dL, urine creatinine 22.8 mg/dL, 24-hour urine volume 2200 mL, 24-hour creatinine clearance 60 ml/min. Urine sodium concentration 105.6 mmol/L, serum sodium 114 mmol/L, sodium clearance: 1.41 ml/min. Fractional sodium excretion was 2.3%. Although the treatment was continued for 6 days, with the same dose of 420 mEq sodium given for each day, the serum sodium concentration reached to 115 mmol/L on day 6. (Totally, 2520 mEq of sodium was given for 6 days). Therefore, hyponatremia was thought to be due to urinary loss of sodium. The fractional sodium excretion of 2.3% supported this. All these findings suggested the diagnosis of renal salt wasting in this patient. We decided to give the patient fludrocortisone (Astonin H 0.1 mg) twice a day orally in addition to sodium chloride tablets (approximately 1.5 gram = 25-30 mmol). During the follow-up of the patient, the both fludrocortisone pills and salt tablets increased to 2 × 2, finally, when reached the level of sodium is above 130 mmol/L, salt tablets were stopped. One thing need to be noted here; hyponatremia did not improve unless giving fludrocortisone. But after this, although more sodium was given during sodium replacement, there was no increase in fractionated sodium excretion, on the contrary, it decreased. On day 14th, Fractional sodium elimination was 1.7%. Serum Na: 133 mmol/L. The patient was advised to take fludrocortisone tablets twice a day orally and was discharged from hospital on day 15th when serum sodium concentration was 138 mmol/L. If a patient with serum cortisol level below 4 mcg/dl have been evaluated as adrenal insufficiency regardless of ACTH level in sera.; additionally, hyperpigmentation and hyponatremia due to salt wasting through the kidneys led us to diagnose. The hyponatremia resolved only after added fludrocortisone. Conclusion However SCLC can give rise euvolemic hyponatremia producing ADH generally, besides, SCLC can cause adrenal insufficiency leading to serious hypovolemic hyponatremia. Diagnose is of crucial importance for correct treatment which can be only achieved by replacing the both sodium and fludrocortisone.

#2136 Hyponatremia as a presenting symptom of secondary adrenal insufficiency induced by immune checkpoint inhibitors

Abstract Background and Aims Endocrinopathies are common complication of treatment with immune checkpoint inhibitors (ICI). Adrenal axis may be affected through either direct adrenal toxicity leading to primary hypoadrenalism or due to pituitary dysfunction resulting in secondary adrenal insufficiency. Patients with secondary insufficiency may have variable presentation and, in some cases, initially present with hyponatremia only. This abstract reports a cohort of patients who developed hyponatremia as initial symptom of secondary adrenal insufficiency. Method After obtaining approval from the institutional review board, medical records of the nephrology service at a large cancer center were reviewed. Patient is well included in the study if they developed moderate (plasma Na <130 mEq/L) and severe (plasma Na <120 mEq/L) hyponatremia during treatment with ICI and met a biochemical criterion for adrenal insufficiency (morning serum cortisol level <3.0 mcg/dL). Results Nine patients who met the criteria were identified (Table 1). There were 5 males and four females. Mean age was 67.6 year. Median number of ICI therapy cycles was 10 but treatment number ranged from 2-84. For patient's would treat with combination of CTLA-4 and PD 1 inhibitors and 5 patients were treated with PD 1 inhibitor alone. Four patients had severe hyponatremia and five presented with moderate hyponatremia. All patients were normotensive on presentation. All patients had low morning cortisol level but only two patients had low ACTH level. All patients had low normal ACTH levels. One patient underwent ACTH stimulation test which was negative. Additionally for patient has had normal thyroid function. Eight patients underwent an MRI and 4 of them had evidence of possible pituitary inflammation. All patients were started on physiologic corticosteroid replacement with prompt resolution of hyponatremia. All patients required ongoing corticosteroid replacement therapy. Conclusion Secondary adrenal insufficiency in the setting of ICI toxicity can present with initial diagnosis of hyponatremia. Patients in this cohort were normotensive on presentation despite adrenal insufficiency and therefore required high index of suspicion for the diagnosis. Most patients in the study also had low normal ACTH levels however responded clinically to treatment with corticosteroid replacement indicating that adrenal sufficiency was the cause of hyponatremia. ACTH test may be falsely negative in these patients if adrenal insufficiency developed less than six weeks prior and adrenal atrophy did not occur yet.

Etiology, Clinical Approach, and Therapeutic Consequences of Hyponatremia

A perturbation in the water balance rather than any change in salt content is the main cause of hyponatremia, the most frequent electrolyte abnormality, defined as a serum sodium concentration <135 mEq/L. Hyponatremia may be divided between mild (Na > 120 mEq/L) or severe (Na < 120 mEq/L) hyponatremia, and is most frequently observed in elderly ICU hospitalized patients. Based on tonicity, hyponatremia may be hypotonic (a decreased concentration of the solute), isotonic, and hypertonic (falsely low sodium). According to the volume of extracellular fluid (ECF), hyponatremia is further divided among hypovolemic, euvolemic, or hypervolemic hyponatremia. Finally, hyponatremia may develop rapidly as acute (<48 h), usually with severe symptoms, or slowly as chronic hyponatremia, usually being asymptomatic or with mild symptoms. Acute severe hyponatremia presents with severe CNS problems, increased hospitalization rates, and mortality. The treatment with 3% sodium chloride and a 100 mL IV bolus based on severity and persistence of symptoms needs careful monitoring. A non-severe hyponatremia may be treated with oral urea. In asymptomatic mild hyponatremia, an adequate solute intake with an initial fluid restriction of 500 mL/d adjusted according to the serum sodium levels is preferred. Vaptans could be considered in patients with high ADH activity regardless of whether they are euvolemic or hypervolemic. In general, the treatment of hyponatremia should be based on the underlying cause, the duration and degree of hyponatremia, the observed symptoms, and volume status of patient.

Pramipexole induced syndrome of inappropriate antidiuretic hormone secretion in a patient with young onset Parkinson’s disease

Abstract Pramipexole, a dopaminergic agonist, has rarely been implicated as a cause of hyponatremia in patients with Parkinson’s disease (PD). Pramipexole-induced stimulation of anti-diuretic hormone results in euvolemic hyponatremia. This is often neglected, and hyponatremia may lead to worsening of the motor symptoms with PD and an unnecessary increase in dopaminergic medications, causing disabling dyskinesias. This case report describes a patient with young-onset PD who developed new-onset hyponatremia due to pramipexole-induced syndrome of inappropriate anti-diuretic hormone within 3 months of starting the drug.

¿Guillain Barre syndrome and inadequate secretion of antidiuretic hormone, is their relationship possible?

Guillain-Barré syndrome (GBS) is a polyradiculoneuropathy of acute onset and the most common cause of acute flaccid paralysis. It is characterized by the appearance of sensory and/or motor symptoms, accompanied by a decrease or absence of muscle stretch reflexes and other symptoms such as facial paralysis, altered eye movements, bulbar symptoms, altered wakefulness, dysautonomia and ataxia. On the other hand, hydroelectrolyte disorders are associated with serious neurological diseases as a poor prognostic factor; the most affected electrolyte is sodium; in fact, hyponatremia is the most common disorder in hospitalized patients, regardless of the cause; in GBS, it is a frequent finding on admission. It is important to recognize hyponatremia, due to its high morbidity and mortality; it is also a marker of an underlying disease. Syndrome of inappropriate secretion of antidiuretic hormone (SSIADH) is the most common cause of hyponatremia and has been associated with Guillain Barre syndrome; in this way, its diagnosis is a challenge for the doctor; finally, below we describe details of a 70-year-old male patient who was admitted to the intensive care unit, with hyponatremia with a SSIHAD, with good subsequent evolution.

Management of Low Sodium in AMU

Hyponatremia is a common finding in acutely ill patients and is defined as serum sodium (Na) level less than 135 mEq/L which is due to a relative excess of water in relation to serum sodium. Reasons for hyponatremia are increase in water intake (hypotonic intravenous fluid therapy or primary polydipsia) or impaired water excretion due to renal failure or increase release of antidiuretic hormone. Optimum management depends on the duration and severity of hyponatremia and involves close monitoring and accurate fluid balance assessment. We will discuss in this article the basics of management, pitfalls to avoid in Hyponatremia and recommended approach based on literature review when reviewing a patient with Hyponatremia, firstly to enquire about the duration of Hyponatremia to differentiate acute from chronic as the threshold for treatment is different, following duration is assessment of severity (clinically by symptoms and signs as well as biochemistry) as severity will affect the management. Following duration and severity the acute physician should assess the volume status of the patient to hypovolemic, euvolemic or hypervolemic Hyponatremia which aids in reaching the possible cause of Hyponatremia and the right treatment.

An enigma of hypothyroidism and hyponatremia coexistence: a nationwide population-based retrospective study

IntroductionHypothyroidism is a rare and possible cause of hyponatremia. However, the clinical epidemiology and risk of mortality (ROM) when they coexist still remain elusive.ObjectivesWe assessed the epidemiology and ROM among index patients with coexisting hypothyroidism and hyponatremia via a national population database.Patients and methodsThis retrospective cohort study utilized Taiwan’s National Health Insurance program database. Distributions of definite sociodemographic factors were analyzed. The annual incidence among the overall group and sex-subgroups was investigated. In addition, potential factors influencing the ROM were also evaluated.ResultsOf 4,549,226 patients from 1998 to 2015, a total of 3,140 index patients with concurrent hypothyroidism and hyponatremia were analyzed. The incidence rate increased tenfold from 1998 to 2015; average annual incidence rate was 174. Among the total participants, 57.1% were women; mean age was 72.6 ± 14.7 years and 88.8% were aged > 55 years. Although average length of stay (LOS) was 13.1 ± 15.4 days, the mortality group had significantly longer LOS than that in the survival group (12.9 days vs 22.2 days). Old age, catastrophic illness, cardiac dysrhythmia, and low hospital hierarchy were independent predictors of hospital mortality. The optimal LOS cutoff value for ROM prediction was 16 days. Index patients with LOS > 16 days increased ROM by 2.3-fold.ConclusionsCoexistent hypothyroidism and hyponatremia is rare, although the incidence increased gradually. Factors influencing the ROM, such as old age, underlying catastrophic status, cardiac dysrhythmia, hospital hierarchy, and LOS should be considered in clinical care.

Improving management of hyponatraemia by increasing urine testing in the emergency department

Hyponatraemia on hospital admission is associated with increased length of stay, healthcare expenditures and mortality. Urine studies collected before fluid or diuretic administration are essential to diagnose the underlying cause...

Hyponatremia and Outcome: Is Severity More Important Than Etiology?

Hyponatremia is the most commonelectrolyte abnormality encountered in a hospital setting, and the data regarding the contribution of hyponatremia to overall mortality are conflicting. The study objective was to determine patients' clinical profiles and outcomes with hyponatremia. This prospective cross-sectional study was conducted at Dayanand Medical College and Hospital, Ludhiana, and included 375 adult patients aged more than 18 years with a confirmed diagnosis of hyponatremia. Patients were subdivided into three groups based on the severity of hyponatremia: mild (130-135 mmol/L), moderate (125-129 mmol/L), and profound (<125 mmol/L). The most common symptom was confusion (57.3%) followed by deep somnolence (40%) and nausea (36.8%). The most common cause of hyponatremia was diuretics (30.7%), followed by the syndrome of inappropriate antidiuretic hormone secretion (SIADH) (17.8%) and chronic liver disease (CLD) (14.1%). The severity of hyponatremia did not significantly influence the outcome. Patients with CLD and chronic kidney disease (CKD) as the etiology of hyponatremia had significantly worse outcomes compared to other causes of hyponatremia. The most common type was hypovolemic hypotonic followed by euvolemic hypotonic and hypervolemia hypotonic hyponatremia. Nearly half of the total deaths were observed in the hypervolemic hyponatremia group and were significantly higher compared to the other two groups (p=0.001). Correction of hyponatremia (i.e., serum sodium >135 mmol/L) was significantly linked with good outcomes (p=0.003). Our study showed that the etiology of hyponatremia was a more important prognostic indicator rather than the severity of hyponatremia. Normalization of serum sodium was associated with improved survival.

Inappropriate therapy of euvolemic hyponatremia, the most frequent type of hyponatremia in SARS-CoV-2 infection, is associated with increased mortality in COVID-19 patients.

Admission hyponatremia, frequent in patients hospitalized for COVID-19, has been associated with increased mortality. However, although euvolemic hyponatremia secondary to the Syndrome of Inappropriate Antidiuresis (SIAD) is the single most common cause of hyponatremia in community-acquired pneumonia (CAP), a thorough and rigorous assessment of the volemia of hyponatremic COVID-19 subjects has yet to be described. We sought to identify factors contributing to mortality and hospital length-of-stay (LOS) in hospitalized COVID-19 patients admitted with hyponatremia, taking volemia into account. Retrospective study of 247 patients admitted with COVID-19 to a tertiary hospital in Madrid, Spain from March 1st through March 30th, 2020, with a glycemia-corrected serum sodium level (SNa) < 135 mmol/L. Variables were collected at admission, at 2nd-3rd day of hospitalization, and ensuing days when hyponatremia persisted. Admission volemia (based on both physical and analytical parameters), therapy, and its adequacy as a function of volemia, were determined. Age: 68 years [56-81]; 39.9% were female. Median admission SNa was 133 mmol/L [131- 134]. Hyponatremia was mild (SNa 131-134 mmol/L) in 188/247 (76%). Volemia was available in 208/247 patients; 57.2% were euvolemic and the rest (42.8%) hypovolemic. Hyponatremia was left untreated in 154/247 (62.3%) patients. Admission therapy was not concordant with volemia in 43/84 (51.2%). In fact, the majority of treated euvolemic patients received incorrect therapy with isotonic saline (37/41, 90.2%), whereas hypovolemics did not (p=0.001). The latter showed higher mortality rates than those receiving adequate or no therapy (36.7% vs. 19% respectively, p=0.023). The administration of isotonic saline to euvolemic hyponatremic subjects was independently associated with an elevation of in-hospital mortality (Odds Ratio: 3.877, 95%; Confidence Interval: 1.25-12.03). Hyponatremia in COVID-19 is predominantly euvolemic. Isotonic saline infusion therapy in euvolemic hyponatremic COVID-19 patients can lead to an increased mortality rate. Thus, an exhaustive and precise volemic assessment of the hyponatremic patient with CAP, particularly when due to COVID-19, is mandatory before instauration of therapy, even when hyponatremia is mild.

Neuroendocrine-induced hyponatremia in patients with traumatic brain injury: a systematic review and meta-analysis of the epidemiology, factors and prognosis

Abstract Traumatic brain injury (TBI) is a common brain dysfunction due to an external force as opposed to disease-induced brain damage. TBI is a leading global cause of high morbidity and mortality rates in the neurosurgical department. It contributes to ~30% of deaths related to brain damage. A common complication of TBIs is hyponatremia secondary to neuroendocrine causes, including syndrome of inappropriate antidiuretic hormone (SIADH), cerebral salt wasting syndrome and adrenal insufficiency. Most recent studies suggest SIADH as the main cause of hyponatremia in TBI. This study aims to evaluate the effects of neuroendocrine-induced hyponatremia on the prognosis of TBI, demonstrate the epidemiology of hyponatremia in patients with TBI, assess all possible etiologies of hyponatremia in TBI, determine the prognostic outcomes of hyponatremia in TBI and determine the effect of hyponatremia on the prognosis of severe and moderate TBI. This study is in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analysis 2020 guideline. A 10-year retrospective analysis of original published studies from January 2013 to January 2023 will be performed. This study will include the adult TBI patients (age ≥ 18 years old) who developed neuroendocrine-induced hyponatremia and original studies, randomized control trials, case controls, cohort studies and studies in English language. This study excludes the pediatric population and animal studies. For information sources, several electronic databases, including EMBASE, Pubmed, SCOPUS and Cochrane, will be searched. No ethical approval is required since the study does not involve human subject participation. However, the study findings will be applied for dissemination at scientific conferences and the manuscript will be submitted for publication to a reputable peer review journal. The research protocol is registered with PROSPERO registration No. CRD42023391854 and is available from: https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42023391854.

#6962 INCIDENCE AND PROGNOSIS OF HYPONATREMIA IN HOSPITALIZED PATIENTS WITH ALCOHOLIC LIVER DISEASE

Abstract Background and Aims Hyponatremia is a common electrolyte disorder in hospitalized patients and has a poor prognosis leading to an increased risk of poor quality of life, morbidity, and mortality. Although the prevalence and prognosis of hyponatremia in advanced liver disease such as liver cirrhosis are well known, no previous studies have been conducted on the prevalence of hyponatremia in early liver disease or alcoholic liver disease (ALD). Therefore, the purpose of this study was to investigate the prevalence and prognosis of hyponatremia in ALD group. Method We performed a retrospective, single centre study of patients admitted to the hepatology department from March 2016 to December 2022. Adults aged 18 years or older were included, and patients with liver cirrhosis, one of the common causes of hyponatremia, were excluded from the study. Based on the electronic medical records, the study was conducted by dividing the ALD group including alcoholic hepatitis and heavy alcoholics into a control group. Results A total of 830 patients were included, hyponatremia (under 135 mmol/L) occurred in 32.2%, and the ALD group showed a significantly higher prevalence than the control group (53.8% vs. 28.6, p&amp;lt;0.001). In addition, the ALD group was statistically significantly higher than the control group in mortality at hospitalization (8.4% vs. 3.9%, p = 0.031) and all-cause mortality (22.7% vs. 12.1%, p = 0.002). The length of hospital stay was significantly longer (13.5±10.9 vs. 10.5±9.1, p = 0.006), and the readmission rate was also higher in the ALD group (39.5% vs. 22.5%, p &amp;lt; 0.001). Kaplan-Meier analysis revealed significantly higher overall survival in the control group than the ALD group (87.9% vs. 77.3% p = 0.002). Conclusion Our study shows that ALD has a higher incidence rate of hyponatremia, which is followed by a poor prognosis, such as an increase in readmission rates, length of hospitalization, and mortality. Therefore, clinicians should realize the importance of electrolyte imbalance in ALD patients and strive to improve prognosis through early and appropriate treatment.

DIURETIC THERAPY – STILL NUMBER 1 REASON FOR HYPONATREMIA

Objective: Hyponatremia is the most common electrolyte imbalance in hospitalized patients. Up to 35% of patients develop hyponatremia during hospitalization. Hypertension is also common in hospitalized patients with prevalence rates up to 72%. We aimed to study the main causes of hyponatremia in hospitalized patients and to investigate the association between hyponatremia and hypertension in this population. Design and method: We included consecutive patients admitted to our hospital between March 2019 and August 2021, with the diagnosis of hyponatremia. We retrospectively analyzed the electronic health records and we collected demographic data, clinical and paraclinical data, hyponatremia etiology and associated comorbidities. We conducted comparative analysis between group without hypertension (Group 1) versus group with hypertension (Group 2). Results: The study population included 397 patients (mean age 71 ± 12 years old, 50,9 % women) with hyponatremia (4,9% of total admissions to our department in the specified period of time) -40,6% mild and 59,4% moderate-severe hyponatremia. The main causes of hyponatremia were diuretic use (37,7%), SARS-COV2 infection (17,1%), NYHA class IV heart failure (12,5%), SARS-COV2 infection associated with diuretic use (10,3%). 21,9% of patients had chronic treatment with psychotropic medication (antidepressants or antipsychotics), 8,6% of patients had chronic treatment with antiepileptic drugs The majority of patients in the study population had hypertension (68,3%). Patients in the hypertensive group were older (72 ± 11 vs 67 ± 15 years old, p&lt;0,001). Mean sodium at hospital admission was lower in group 2 (125,9 vs 127,8 p = 0,01). Hyponatremic encephalopathy was more common in group 2 (15,9% vs 4,0%, p = 0,001). Diuretic use was also more prevalent in hypertensive group (56,3% vs 31,0%, p&lt;0,001). Loop diuretic use was similar between groups (38,5%-Group 1 vs 32,5% - Group 2, p = 0,47), but thiazide-like diuretic use was more common in Group 2 (46,8% vs 20,5%, p = 0,003). Conclusions: The most common etiology of hyponatremia in the internal medicine department of an emergency hospital was diuretic use. Hypertension was associated with older age, lower sodium at hospital admission, hyponatremic encephalopathy and thiazide-like diuretic use in this population.

Abstract #1405536: Hyponatremia After Placement of an External Lumbar Drain Following Transsphenoidal Surgery in a Patient with Preoperative Diabetes Insipidus

Hypernatremia due to diabetes insipidus (DI) is perhaps the most anticipated electrolyte abnormality after transsphenoidal surgery (TSS), but hyponatremia is more common and occurs in over 15% of patients undergoing TSS. Postoperative placement of an external lumbar drain (ELD) is a well-known risk factor for hyponatremia following TSS. We present an unusual case of refractory hyponatremia occurring after ELD placement in a patient with preoperative DI. A 68-year-old male underwent TSS for resection of a recurrent sella meningioma. History was notable for multiple recurrences and resections of the tumor, and the patient was treated for longstanding central DI and hypopituitarism (>10 y). Surgery was complicated by bleeding, requiring placement of an ELD. Preoperative serum sodium levels were in the reference range (136-145 mM), but within 48 h of ELD placement, serum sodium level fell to 127 mM. Spot urine sodium level and osmolality were <10 mM and 162 mOsm/kg, respectively. The patient received stress dose glucocorticoids after surgery, and free T4 level was in the reference range (0.5-1.3 ng/dL). Other causes of hyponatremia and pseudohyponatremia, including hyperglycemia, renal tubular acidosis, paraproteinemia, and hyperlipidemia were excluded. While the lumbar drain was in place, serum sodium levels remained 125-129 mM despite decreasing the amount and frequency of DDAVP doses for treatment of preoperative central DI. After the ELD was removed, hyponatremia resolved within 48 h, and the patient was discharged home with a serum sodium level of 140 mM on oral DDAVP (0.1 mg BID) prescribed prior to surgery. In a series of over 300 adults undergoing TSS, placement of an ELD accounted for almost half of hyponatremia cases. Cerebral salt wasting syndrome (CSWS) and syndrome of inappropriate antidiuretic hormone (SIADH) are identified as the most common causes of ELD-induced hyponatremia, though undetectable urine sodium level in this case excludes CSWS. Spot urine osmolality was surprisingly high (>100 mOsm/kg) for the patient’s longstanding central DI, appearing to indicate SIADH as the etiology of hyponatremia. The patient likely had partial central DI, and persistent hyponatremia after placement of the ELD despite significant reductions of DDAVP doses appears to be best explained by release of endogenous ADH by surviving magnocellular neurons of the supraoptic nucleus in the hypothalamus superimposed on treatment with DDAVP. This case demonstrates that ELD-induced hyponatremia is possible in patients treated for central DI prior to TSS and likely indicates only a partial deficit of endogenous ADH secretion.

Severe hyponatremia as an atypical manifestation of pituitary macroadenoma: a case report.

We present a case of a 45-year-old woman who presented with symptoms of lethargy, vomiting, altered sensorium, and seizure. Her initial sodium level was 107mEq/l, plasma and urinary osmolality were 250 and 455mOsm/kg, respectively, and her urine sodium level was 141mEq/day, suggestive of hyponatremia due to SIADH. MRI scan of the brain revealed approximately 14×13×11mm pituitary mass. Prolactin and cortisol levels were 41.1ng/ml and 5.65μg/dl, respectively. Hyponatremia can result from various diseases, making it hard to identify the cause. A pituitary adenoma is a rare cause of hyponatremia due to SIADH. Pituitary adenoma rarely might be the cause of SIADH presenting as severe hyponatremia. So, in case of hyponatremia due to SIADH, clinicians should keep pituitary adenoma as well in their differential diagnoses.

Intractable hyponatremia secondary to syndrome of inappropriate antidiuresis complicated with empty sella: A case report

Hyponatremia is a common electrolyte disorder in elderly critically ill patients, and it may be associated with poor outcomes, higher morbidity, and mortality. Syndrome of inappropriate antidiuresis (SIAD) is one of the main causes of hyponatremia, with an insidious onset that is highly misdiagnosed. Primary empty sella lesions are specific, mostly asymptomatic, and easily overlooked. SIAD combined with empty sella is much rarer in clinic, this article focuses on the diagnosis and management of an elderly patient with intractable hyponatremia secondary to syndrome of inappropriate antidiuresis complicated with empty sella. An 85-year-old male patient with severe pneumonia presented with progressive and intractable hyponatremia. The patient had clinical signs of persistent hyponatremia, low plasma osmolality, elevated urinary sodium excretion, and hyponatremia that worsened with increased intravenous rehydration and was effective with appropriate fluid restriction. The diagnosis of SIAD combined with empty sella was made in combination with the findings of the pituitary and its target gland function. Numerous screenings were performed to clarify the cause of hyponatremia. His overall condition was poor due to recurrent episodes of hospital-acquired pneumonia. We treated with ventilation support, circulatory support, nutritional support, anti-infection, and continuous correction of electrolyte imbalance. His hyponatremia gradually improved through aggressive infection control, appropriate fluid restriction (intake controlled at 1500-2000mL/d), continuous electrolyte correction, supplementation with hypertonic salt solution, and potassium replacement therapy. Electrolyte disorders, especially hyponatremia, are very common in critically ill patients, but the etiology of hyponatremia is challenging to diagnose and treat, and timely attention and proper diagnosis of SIAD and individualized treatment are the significance of this article.

Haptoglobin-Related Protein without Signal Peptide as Biomarker of Renal Salt Wasting in Hyponatremia, Hyponatremia-Related Diseases and as New Syndrome in Alzheimer’s Disease

The application of pathophysiologic tenets has created significant changes in our approach to hyponatremia and hyponatremia-related conditions. This new approach incorporated the determination of fractional excretion (FE) of urate before and after the correction of hyponatremia and the response to isotonic saline infusion to differentiate the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) from renal salt wasting (RSW). FEurate simplified the identification of the different causes of hyponatremia, especially the diagnosis of a reset osmostat and Addison's disease. Differentiating SIADH from RSW has been extremely difficult because both syndromes present with identical clinical parameters, which could be overcome by successfully carrying out the difficult protocol of this new approach. A study of 62 hyponatremic patients from the general medical wards of the hospital identified 17 (27%) to have SIADH, 19 (31%) with reset osmostat, and 24 (38%) with RSW with 21 of these RSW patients presenting without clinical evidence of cerebral disease to warrant changing the nomenclature from cerebral to renal salt wasting. The natriuretic activity found in the plasma of 21 and 18 patients with neurosurgical and Alzheimer's disease, respectively, was later identified as haptoglobin-related protein without signal peptide (HPRWSP). The high prevalence of RSW creates a therapeutic dilemma of deciding whether to water-restrict water-logged patients with SIADH as compared to administering saline to volume-depleted patients with RSW. Future studies will hopefully achieve the following: 1. Abandon the ineffective volume approach; 2. Develop HPRWSP as a biomarker to identify hyponatremic and a projected large number of normonatremic patients at risk of developing RSW, including Alzheimer's disease; 3. Facilitate differentiating SIADH from RSW on the first encounter and improve clinical outcomes.