Syndrome Of Antidiuretic Hormone Secretion Research Articles

Prevalence and Aetiology of Syndrome of Inappropriate Antidiuretic Hormone in Hyponatraemia: A Cross-sectional Study

Introduction: Hyponatraemia is a frequently occurring electrolyte abnormality. Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) is one of the common causes of hyponatraemia. SIADH is a disorder of impaired water excretion caused by the inability to suppress the secretion of Antidiuretic Hormone (ADH). The importance of determining the cause of hyponatraemia as SIADH is not only to seek the aetiology of SIADH but also to treat appropriately. Aim: To determine the prevalence of SIADH in patients with hyponatraemia and its causes in these patients. Materials and Methods: A cross-sectional study was conducted in the Department of General Medicine at Jubilee Mission Medical College and Hospital, Thrissur, Kerala, India. The study duration was one year and six months, from December 2014 to June 2016. A total of 100 individuals over the age of 18, who were admitted with serum sodium levels under 135 mEq/L, were chosen. Data on the causes of hyponatraemia and SIADH, laboratory evaluations, and assessments based on SIADH criteria were gathered using a structured proforma. The primary outcome variables included the aetiology of SIADH and the causes of hyponatraemia. Frequency and percentages were used to represent the data. The data were analysed using MS Excel. Results: Among 100 patients, the maximum number of patients with hyponatraemia were in the 59-78 years age group. Fortytwo (42) had severe hyponatraemia (Na < 120 mmol/L). The most common cause of hyponatraemia was drug intake (diuretics + antihypertensives), which constituted 42 (42%) of the total 100 patients, followed by SIADH in 33 (33%) patients. Among the aetiologies of SIADH, cerebrovascular accident was the most common (9/100), followed by pneumonia and Selective Serotonin Reuptake Inhibitors (SSRIs) in five patients each. Among the non neurological symptoms, vomiting was the most common symptom in 28 (28%) patients, followed by lethargy in 15 (15%). Among the neurological symptoms associated with hyponatraemia, confusion was the predominant one seen in 10 (10%) patients, followed by drowsiness in 7 (7%). Conclusion: SIADH is an important cause of hyponatraemia with a high prevalence. The prevalence of SIADH in hyponatraemic patients was 33%. Among the aetiologies of SIADH, cerebrovascular accident was the most common.

Aquaporins in Edema.

One of the most prevalent indications of water-electrolyte imbalance is edema. Aquaporins (AQPs) are a protein family that can function as water channels. Osmoregulation and body water homeostasis are dependent on the regulation of AQPs. Human kidneys contain nine AQPs, five of which have been demonstrated to have a role in body water balance: AQP1, AQP2, AQP3, AQP4, and AQP7. Water imbalance is connected with AQP dysfunction. Hyponatremia with elevated AQP levels can accompany edema, which can be caused by disorders with low effective circulating blood volume and systemic vasodilation, such as congestive heart failure (CHF), hepatic cirrhosis, or the syndrome of incorrect antidiuretic hormone secretion (SIADH). In CHF, upregulation of AQP2 expression and targeting is critical for water retention. AQP2 is also involved in aberrant water retention and the formation of ascites in cirrhosis of the liver. Furthermore, water retention and hyponatremia in SIADH are caused by increased expression of AQP2 in the collecting duct. Fluid restriction, demeclocycline, and vasopressin type-2 receptor antagonists are widely utilized to treat edema. The relationship between AQPs and edema is discussed in this chapter.

Clinical, Biochemical, and Outcome Profile of Hyponatremia in Geriatric and Non-Geriatric Individuals Admitted to a Tertiary Care Centre: A Prospective Cohort Study

Introduction: Hyponatremia is one of the most common electrolyte disturbances encountered in medical wards, occurring in up to 22% of hospitalised patients. Timely recognition and correction of hyponatremia in hospitalised patients may help decrease in-hospital mortality and symptom severity, reduce the need for intensive hospital care, decrease the duration of hospitalisation and associated costs, and improve the treatment of underlying co-morbid conditions and patient’s quality of life. Aim: To compare the clinical presentation, aetiology, biochemical profile, management strategies, and outcomes of hyponatremia in geriatric and non-geriatric individuals admitted to a tertiary care centre. Materials and Methods: This prospective cohort study was conducted in the Department of General Medicine at Mahatma Gandhi Medical College and Research Institute, Pondicherry, India, from March 2021 to September 2022. A total of 166 subjects (83 geriatric and 83 non-geriatric patients) receiving inpatient services with hyponatremia were enrolled in the study by consecutive sampling. Patients over 18 years of age admitted to the Department of General Medicine with serum sodium levels below 135 mEq/L were included. Comparison of both the groups were done based on clinical presentation, laboratory values, co-morbidities, prescription drugs taken, aetiology, treatment given, and outcomes. For quantitative variables, mean, standard deviation, and independent t-tests were used, while percentages were used for qualitative variables. Results: The majority of subjects in the non-geriatric group belonged to the age group of 50-59 years, with a mean age of 50.7 years. In the geriatric group, most subjects were in the age group of 65-74 years, with a mean age of 74.5 years. The most common cause of hyponatremia in both groups was Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH), with 32 (38.6%) cases in the non-geriatric group and 27 (32.5%) cases in the geriatric group. This was followed by volume overload in the non-geriatric group, with 14 (16.9%) cases, and drug-induced hyponatremia in the geriatric group, with 22 (26.5%) cases. The most common drug causing hyponatremia was furosemide in both groups. In non-geriatric patients, the most common symptom was giddiness, with 28 (34.1%) cases, while in geriatric patients, it was nausea/vomiting, with 25 (30.1%) cases. Tolvaptan was the most common treatment used in both groups, with 12 (92.3%) of patients with mild hyponatremia receiving it in the non-geriatric group (p=0.042), and 46 (55.4%) patients in the geriatric group, with most of them having moderate hyponatremia (26, 86.7%, p<0.001). Conclusion: The results of the non-geriatric and geriatric groups were similar in terms of clinical presentation, biochemical parameters, management strategies, and outcome of hyponatremia. However, the aetiology of hyponatremia appeared to be different. The most common cause of hyponatremia was SIADH in both groups, followed by volume overload in the non-geriatric group and drug-induced hyponatremia in the geriatric group.

Hyponatremia in malignant neoplasia: A case report

Hyponatremia is a frequent electrolyte imbalance with diverse etiology that may occur secondary to chemotherapy or autoimmune pathologies. We report the case of a 76-years-old female who presented for symptoms of severe hyponatremia like digestive intolerance, nausea, vomiting, generalized muscle weakness and vertigo, with a serum sodium level of 110 mEq/L. The patient was known with multiple cardiovascular and malignant comorbidities, being diagnosed with a right breast neoplasm with right radical mastectomy and axillary lymphadenectomy. Subsequently, multiple adenopathies were detected, which is why the patient followed several series of chemotherapy with trastuzumab and capecitabinum. These drugs can cause side effects, such as xerophthalmia, xerostomia, which are also frequently encountered in autoimmune pathologies. Hyponatremia is one of the most frequent side effects of capecitabinum. All these side reactions were investigated later, thus following the immunological tests, the diagnosis of Sjogren's syndrome was established. After ruling out other causes, it was established that hyponatremia appeared secondary to the recent administration of capecitabinum or within a syndrome of inappropriate antidiuretic hormone secretion (SIADH), which can be the result of a Sjogren's syndrome.

Recurrent Hyponatremia: Levetiracetam - An Uncommon Cause.

Dear Editor, Hyponatremia can be an adverse drug reaction with the use of some of the anti-seizure medications (ASM). Carbamazepine and oxcarbazepine are the most common ASMs which induce hyponatremia. Rarely sodium valproate, eslicarbazepine, lamotrigine, levetiracetam, and gabapentin have also been reported to cause hyponatremia.[1] We report a case of Levetiracetam induced hyponatremia and review the English literature of similar cases. A 50-year-old male had traumatic brain injury in November 2015 and neuroimaging was normal. He was started on prophylactic levetiracetam at another facility. Since then, he had three admissions for hyponatremia: First admission was for acute symptomatic seizures due to hyponatremia, serum sodium of 118 mmol/L; second admission in February 2016 for dizziness, serum sodium 131 mmol/L; and third admission during April 2016 for drowsiness, serum sodium 108 mmol/L [Table 1]. During the latter two admissions, the work-up for hyponatremia was suggestive of syndrome of inappropriate antidiuretic hormone secretion (SIADH). During the first admission, patient was on levetiracetam 500 mg q12h and the dose was escalated to 1000 mg q12h at discharge. Patient was started on tolvaptan 15 mg q24h at discharge in the first admission (25.12.2015). During his subsequent admissions, workup for other causes of hyponatremia was negative. He was continued with tolvaptan intermittently. Review of the case records and drug chart suggested possible relation between hyponatremia and levetiracetam, a diagnosis of levetiracetam induced hyponatremia was considered and levetiracetam was discontinued. Since then, he had no further episode of hyponatremia. Patient was not started on any ASM as it is not our practice to use ASMs for primary prophylaxis in traumatic brain injury.Table 1: Admission profile of the patientIn this patient, diagnostic workup suggested that SIADH was the possible mechanism for hyponatremia. He had a mild closed traumatic brain injury and normal brain imaging. This clinical scenario is very unlikely to cause SIADH. Workup for other causes of hyponatremia was negative. When levetiracetam was discontinued patient had no further episodes of hyponatremia. On Naranjo Adverse Drug Reaction Probability Scale[2] this patient had a score of 7 suggesting levetiracetam being the “probable” culprit responsible for hyponatremia. Review of English literature revealed report of four patients with levetiracetam induced hyponatremia [Table 2]. In four patients, including the present case SIADH was the mechanism of hyponatremia. There are no specific clinical characteristics which are common among these 5 cases. In all the patients, hyponatremia was corrected after withdrawing levetiracetam. In patient “3” in addition to levetiracetam, hydrochlorothiazide would have added to the misery of hyponatremia.Table 2: Characteristics of the patientsIn conclusion this case illustrates that chronic hyponatremia in a patient with epilepsy on ASMs, one should check the ASM list to exclude the possible drug that can be associated with hyponatremia. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.

Oxcarbazepine-induced syndrome of inappropriate antidiuretic hormone secretion in a trigeminal neuralgia: A case report

Oxcarbazepine-induced syndrome of inappropriate antidiuretic hormone secretion in a trigeminal neuralgia: A case report

Cerebral Salt Wasting Syndrome Associated with Status Epilepticus

Cerebral salt wasting syndrome (CSWS) is defined as a renal loss of sodium in cerebral disorders causing hyponatremia and loss of extracellular fluid volume. Similar laboratory findings may be seen in other conditions such as syndrome of inappropriate antidiuretic hormone secretion (SIADH). A 58-year-old male visited our emergency department because of the sudden development of seizures during sleep. Magnetic resonance imaging revealed subtle high signal intensity in the right hippocampus on diffusion-weighted imaging. Ictal rhythmic discharges were observed in the concordant area. Altered metal status, polyuria and laboratory test findings including hyponatremia were compatible with CSWS. After hydration and salt replacement, his mental state and hyponatremia gradually recovered. For diagnosing CSWS, meticulous physical examinations including analysis of fluid balance are essential. CSWS should be considered in patients with hyponatremia and polyuria. Accurate diagnosis of CSWS and SIADH is crucial as the treatment plans for these two conditions are completely different.

Hyponatraemia – diagnostic difficulties in 2.5-year-old boy with nephrogenic syndrome of inappropriate antidiuresis. Case report

Normal sodium levels in the extracellular fluid are in the range of 135–145 mmol/L. Low serum sodium (hyponatraemia) is a common water and electrolyte balance disorder. Dehydration and overhydration are the most common causes of hyponatraemia in children. This paper describes a case of a 2.5-year-old boy admitted to the paediatric ward due to pneumonia. The child showed reluctance to fluid intake, hypoosmolar hyponatraemia with hypouricaemia, and increased urinary sodium excretion in the absence of abnormalities in hydration status. He had a family history of persistent hyponatraemia and hypertension in his grandfather. After excluding pituitary, thyroid, adrenal cortex pathologies, kidney disfunction, and proliferative processes in the differential diagnosis, cerebral salt wasting syndrome, the syndrome of inappropriate secretion of antidiuretic hormone and the renal-related syndrome of inappropriate antidiuresis were taken into account. The aim of the study was to discuss the differential diagnosis of chronic euvolemic hyponatraemia and to draw attention to the need for genetic testing for the nephrogenic syndrome of inappropriate antidiuretic hormone secretion caused by activating point mutations of the vasopressin 2 receptor gene (V2R).

Kidney collecting duct cells make vasopressin in response to NaCl-induced hypertonicity.

Vasopressin has traditionally been thought to be produced by the neurohypophyseal system and then released into the circulation where it regulates water homeostasis. The questions of whether vasopressin could be produced outside of the brain and if the kidney could be a source of vasopressin are raised by the syndrome of inappropriate antidiuretic hormone secretion (vasopressin). We found that mouse and human kidneys expressed vasopressin mRNA. Using an antibody that detects preprovasopressin, we found that immunoreactive preprovasopressin protein was found in mouse and human kidneys. Moreover, we found that murine collecting duct cells made biologically active vasopressin, which increased in response to NaCl-mediated hypertonicity, and that water restriction increased the abundance of kidney-derived vasopressin mRNA and protein expression in mouse kidneys. Thus, we provide evidence of biologically active production of kidney-derived vasopressin in kidney tubular epithelial cells.

227: A CASE REPORT ON HEATSTROKE ASSOCIATED WITH SIADH

Introduction: Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is known to be associated with central nervous system disorders such as stroke, infectious diseases, trauma, and neoplastic lesions. However, its association with heat stroke has not been reported. In this report, we describe a case of heat stroke complicated with SIADH. Description: A 54-year-old man had no history of heat stroke. He was living in a non-air-conditioned room during a heat wave with temperatures exceeding 35 °C every day. He had been feeling unwell since the previous day and was confined to the toilet in his home since breakfast. A few hours later, he collapsed and had convulsions that led to a call for emergency medical assistance. When he came to the hospital, his convulsions had aborted and his vital signs were: pulse 124 times/min, blood pressure 129/77 mmHg, respiratory rate 30 times/min, SpO2 97% (room air), and rectal temperature 42.0 °C. His level of consciousness had decreased to E1V1M4/GCS. Blood tests showed a mildly elevated inflammatory response and hyponaemia of Na 110.4 mEq/L. CT and MRI scans showed no intracranial lesions. The patient’s loss of consciousness was attributed to heat stroke and hyponaemia. Aggressive cooling and fluid infusion were performed and the patient was admitted in the ICU. Physical examination revealed no dehydration. The laboratory test showed plasma osmolality 244 mOsm/kg, urine osmolality 423 mOsm/kg, urinary Na concentration 99 mEq/L, ADH 43.1 pg/ml, and cortisol 46.8 μg/dl, consistent with a diagnosis of SIADH. The patient serum Na levels recovered to 136.1 mEq/L on the 7th day. On the 11th day, his level of consciousness improved to E4V4M6/GCS, and he was transferred to the hospital for rehabilitation on the 13th day. Discussion: Heat stroke can cause central nervous system (CNS) disorders via unclear mechanisms. It can cause cerebral edema, neuroinflammation, and oxidative stress. Their mechanisms are like those of neuropathy caused by trauma and inflammation, suggesting that heat stroke can cause SIADH. In this patient, heat stroke was complicated by SIADH, rendering the patient severely hyponaemic. In this case, there was no other possible cause of SIADH other than CNS damage due to heat stroke, suggesting an association between heat stroke and SIADH.

Secondary adrenal insufficiency in patient with COVID-19 and head and neck cancer

Syndrome of inappropriate antidiuretic hormone (SIADH) secretion is an endocrinological disorder which occurs when there is an evidence of continued antidiuretic hormone (ADH) secretion in the absence of an appropriate osmotic volume stimulus. Most commonly it is caused by different types of cancer or medications (eg. diuretics, antidepressants, antipsychotics...). Secondary adrenal insufficiency is caused by the insufficient adrenocorticotropic hormone (ACTH) secretion and cortisol production. In the hypocortisolism, the inhibitory mechanism on ADH secretion vanishes causing increased ADH secretion and leading to SIADH-like state. Both conditions, SIADH and hypocortisolism, manifest in euvolemic hyponatremia, however, its cause can be misdiagnosed and result in an inadequate treatment and potentially fatal outcome. Our case is about fifty-seven-year-old male patient who was treated with chemoradiotherapy for hematological malignancy of the oropharynx and who presented with severe hyponatremia se-veral times that almost ended fatally. Considering his malignant disease, patient was diagnosed with SIADH as a cause of hypona-tremia and was treated with hypertonic saline fluids and fluid intake restriction. However, after having suffered Covid-19 infection the patient was given glucocorticoids according to the protocol at the time. The sodium levels finally corrected, and the secondary adrenal insufficiency has been declared as the real cause of hyponatremia. SIADH is often thought to be the cause of hyponatremia in patients with malignant disease. However, SIADH represents a diagnosis of exclusion. Before making a final diagnosis, thyroid and secondary adrenal insufficiency must be ruled out. Moreover, secondary adrenal insufficiency imitates SIADH and results in euvolemic hyponatremia but the management and potential outcomes of these two conditions differ significantly. In patients who have been previously treated for malignancies with the treatment options that increase the risk of adrenal insufficiency (chemotherapy, neck or skull base radiotherapy, immunotherapy), adrenal reserve must be evaluated. If introduced, the glucocorticoid therapy should be carefully deescalated in these patients because of the risk of previously unrecognized adrenal insufficiency. This especially applies to conditions that include glucocorticoid therapy in the treatment protocol, such as Covid-19 infection.

PMON318 Nephrogenic syndrome of inappropriate antidiuresis in a 19 months old child with gross developmental delay

Abstract Case report 19 months old African American boy with nonsignificant past medical history presented with inability to walk, hypotonia chewing difficulties and speech delay. Initial laboratory evaluations demonstrated serum hyponatremia of 120-129 mEq/dl, low serum osmolality 261 mosm/kg (normal serum osmolality 275-295 mosm/kg) with inappropriately high urine osmolality 445 mosm/kg) (normal urine osmolality 300-1000 mosm/kg). Blood work for thyroid, adrenal, and pituitary function was unremarkable. Vasopressin level of 2.4 pg/ml (normal 0.0 - 4.7 pg/mL) did not support the diagnosis of Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH). Fludrocortisone challenge test ruled out aldosterone deficiency with insufficient decrease in urine sodium and no response in serum sodium. Renal ultrasound and brain MRI were normal. Genetic testing revealed AVPR2 X-linked mutation c.409C>T p.R137C, consistent with nephrogenic syndrome of inappropriate antidiuresis (NSIAD). The patient was discharged on sodium chloride tablets 2g every 8 hours and remained stable, asymptomatic. One month after discharge patient showed significant neurological improvement. Discussion Sodium is known to play a significant role in growth and maturation of the whole body, especially of the nervous system. Moderate (120-129 mEq/L) to severe (<120 mEq/L) hyponatremia can present with nausea, malaise, headache, lethargy, motor and speech delay, seizures and even death due to brain herniation. Normal fluid and electrolyte balance is achieved by the thirst mechanism and free water excretion in kidneys. This is mediated by Vasopressin, which acts through V2R receptor in distal renal collecting duct. Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is the most common cause of hyponatremia. Reset osmostat syndrome with a congenitally low serum osmolality threshold is one of the rare disorders on the differential. Hereditary nephrogenic syndrome of inappropriate antidiuresis is very rare mutation in vasopressin receptor, which clinically resembles SIADH except for normal/low vasopressin levels in set of hyponatremia. It causes gain of function and inappropriately high water retention. Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30 p.m.

PMON39 A Perfect Storm – Multiple Causes of Hyponatremia in Patient With Pituitary Macroadenoma

Abstract Introduction Adrenal insufficiency is a life threatening condition, and prompt diagnosis and treatment are necessary. Here we present a case of hyponatremia which was thought to be multifactorial due to secondary adrenal insufficiency in the setting of a pituitary macro-adenoma, central hypothyroidism, SIADH in the setting of nausea as well as analgesic use. Case presentation A 23 y.o female patient presented to the hospital with headaches. MRI of the head revealed a 2.2 cm pituitary mass abutting the optic chiasm with no edema and no need for urgent neurosurgical intervention. Outpatient endocrine workup demonstrated following labs: Na 135 mmol/l (ref range 135 - 145), afternoon cortisol 9.3 mcg/dl (ref range 5.0 - 23.0), ACTH 19 pg/ml (ref range 7.2-63), GH 3.8 ng/ml (ref range <=7.1), Prolactin 16.0 ng/ml (ref range 4.8 - 23.3). Due to persistent headaches, she was taking high doses of Naproxen, which resulted in nausea and vomiting, and led to another ED visit. At this time, she was found to have Na 117 mmol/l, Serum osmolality 246 mOsm/kg (re range 285–295), Urine osmolality 554 mOsm/kg (ref range 40 - 1,400), Urine Na 146 mmol/L. TSH was 0.16 mIU/ml (ref range 0.27 - 4.20) and free T4 was 0.49 ng/dl (ref range 0.80 - 1.90). Endocrine was consulted and the pathogenesis for hyponatremia was thought to be multifactorial including central adrenal insufficiency masked by central hypothyroidism. Her cortisol levels as detailed above were done early afternoon and could not exclude at least some degree of central adrenal insufficiency. Additionally, hypothyroid state can significantly decrease metabolism of cortisol thus preventing acute drop in cortisol levels. She also seemed to have concomitant syndrome of inappropriate antidiuretic hormone secretion (SIADH), driven by both the pituitary tumor as well as nausea and vomiting. On top of that for her severe progressive headaches she was treated with non-steroidal anti-inflammatory agents and tramadol, both known to associate with hyponatremia. She was started on intravenous hydrocortisone, and subsequently oral levothyroxine. She had improvement in her sodium levels and did not require Tolvaptan. She was discharged on hydrocortisone and levothyroxine with outpatient endocrine and neurosurgery follow up. She is currently awaiting neurosurgical intervention. Discussion Secondary adrenal insufficiency is more common than primary adrenal insufficiency. Establishing the diagnosis of secondary adrenal insufficiency is challenging as it is not typically associated with classical signs and symptoms of adrenal insufficiency. Clinical manifestations tend to be more indolent as they result from glucocorticoid deficiency only and there is preservation of the aldosterone and adrenal androgen axis. What makes our patient interesting is the several factors as mentioned above which contributed to her severe hyponatremia. Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30 p.m.

ODP371 A Nationwide Analysis of Hospitalization trends of Syndrome of inappropriate anti-diuretic hormone secretion (SIADH) with comorbid Atrial Fibrillation

Abstract Syndrome of inappropriate anti-diuretic hormone secretion (SIADH) is a disease of unsuppressed secretion of anti-diuretic hormone (ADH) and its continued action on the Vasopressin (V2) receptors. It is characterized by hyponatremia in a setting of hypervolemia or euvolemia. In this study, we aimed to identify and compare demographic characteristics, adverse outcomes, and complications of SIADH hospitalizations with and without comorbid atrial fibrillation (AF). We analyzed the Nationwide Inpatient Sample (NIS) for 2019 to identify all adult (≥18 years) hospitalizations with a principal diagnosis of SIADH using the ICD-10-CM code (E22.2). Patients <18 years of age were excluded from the analysis. The study cohort was further divided based on the presence of absence of AF. Demographic and hospitalization characteristics were highlighted. Using a multivariate regression analysis adjusting for age, sex, race, primary payer, median household income by zip code, Carlson Comorbidity Index (CCI), hospital location, bed-size, and teaching status, inpatient outcomes such as inpatient mortality, rates of septic shock, acute myocardial infarction (AMI), acute respiratory failure (ARF), acute renal failure (AKI), and acute pulmonary edema (APE) were determined. All p-values< 0. 05 were considered statistically significant. In 2019, of the 39,110 hospitalizations for SIADH, 18.5% of the patients had comorbid AF. SIADH hospitalizations with AF were older (80.4 vs 70.1 years, p<0. 001, predominantly White and a higher proportion of patients with CCI >2 compared to the non-AF cohort. Although there was a higher proportion of females in the AF cohort (61.4% vs 63.1%, p=0.252), we did not find a statistically significant difference for gender between the two subgroups. SIADH hospitalizations with AF were associated with higher adjusted odds ratio (aOR) of inpatient mortality (2.1 vs 0.9%, aOR: 2.45, p<0. 001), increased length of stay (LOS), (5.8 vs 4.8 days, p<0. 001) and increased mean hospitalization cost (THC) ($12,284 vs $10,340, p <0. 001) compared to the non-AF cohort. Furthermore, compared to the non-AF cohort, we noted higher odds of septic shock (0.6 vs 0.3%, aOR: 3.35, p=0. 007) and ARF (11.2 vs 6.5%, aOR: 1.88, p<0. 001) for the AF cohort; however, we did not find a statistically significant difference in the odds of CVA, AKI or AMI between the two groups. Patients hospitalized with SIADH, and comorbid AF had higher inpatient mortality, LOS, THC, which may be secondary to multiple electrolyte abnormalities and fluid imbalances associated with SIADH leading to a worsening of the AF. Furthermore, these patients had higher odds of septic shock and ARF. Hence, it is vital to appropriately manage AF in patients with SIADH to prevent adverse outcomes and decrease the burden on the United States healthcare system. Presentation: No date and time listed

PSUN296 Impact of Diabetes Mellitus on Outcomes of Hospitalizations for SIADH

Abstract Introduction Diabetes mellitus (DM) is known to cause hyponatremia via multiple mechanisms and is often a confounder in the diagnosis of the syndrome of inappropriate anti-diuretic hormone secretion (SIADH). However, not much is known about the prevalence of DM in patients with SIADH or the effect it has on outcomes of hospitalizations for SIADH. Method: Data was extracted from the US Nationwide Inpatient Sample (NIS) for 2019. The NIS contains hospital discharge information estimating yearly US hospitalizations. We included hospitalizations with a principal discharge diagnostic code for SIADH using the ICD-10-CM code (E22.2). We excluded hospitalizations of patients less than 18 years. This cohort was divided based on the secondary diagnosis of diabetes mellitus (DM). We compared inpatient mortality rates, mean length of hospital stay (LOS), mean hospitalization cost (THC), and rates of septic shock, acute myocardial infarction (AMI), acute respiratory failure (ARF), acute renal failure (AKI), and acute pulmonary edema (PE) between the subgroups. Adjustments were made for age, sex, race, primary payer, median household income by zip code, Charlson Comorbidity Index (CCI), hospital location, bed-size, and teaching status using multivariate regression analysis. Statistical significance was set at a p-value < 0.05. Results In 2019, there were 39,110 hospitalizations with SIADH as the reason for the admission. Comorbid DM was prevalent in 25.4% of these admissions. A higher proportion of hospitalizations involved females, with no significant difference between both cohorts (62.3 vs 60.1%, p=0.084). Patients with DM had a higher mean age (73.3±12 vs 72.4±13.8 years, p=0.005), a higher proportion of CCI >2, and a higher proportion of ethnic minorities. In patients with SIADH, DM was associated with no mortality difference (1.2% vs 0.9%, p=0.317) and no difference in LOS (4.9 vs 5.1 days, p=0.328) despite increased THC (10,873 vs 10,641 US$, p =0.03). Comorbid DM was associated with lower odds of AMI (0.4 vs 0.8%, aOR: 0.315, p=0.002), PE (0.15 vs 0.4%, aOR: 0.22, p=0.012) and ARF (6.8% vs 7.5%, aOR: 0.77, p=0.016), higher odds of AKI (15.9 vs 10.7, aOR: 1.23, p=0.008), with no significant difference in odds of septic shock or CVA. Conclusions Comorbid DM was associated with no difference in mortality or LOS despite an association with increased THC and AKI in hospitalizations of patients with SIADH. Notably, DM also appeared to lower the odds of AMI, PE, and ARF in this cohort of patients. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.

PSUN119 Obesity As An Independent Factor In Outcome Of SIADH Hospitalizations

Abstract Introduction Several comorbidities have been associated with the syndrome of inappropriate anti-diuretic hormone secretion (SIADH). However, not much literature documents an association between SIADH and obesity, and there is a marked paucity of research documenting the impact of obesity on outcomes in patients hospitalized with SIADH. Method We extracted data from the US Nationwide Inpatient Sample (NIS) for 2019. The NIS contains hospital discharge information estimating yearly US hospitalizations. We included hospitalizations with a principal discharge diagnostic code for SIADH using the ICD-10-CM code (E22.2). The study excluded hospitalizations of patients less than 18 years. This cohort was divided based on the secondary diagnosis of obesity. Outcomes included comparing inpatient mortality rates, mean length of hospital stay (LOS), mean hospitalization cost (THC), rates of septic shock, acute myocardial infarction (AMI), acute respiratory failure (ARF), acute renal failure (AKI), acute pulmonary edema (PE) between the subgroups. An adjustment was made for age, sex, race, primary payer, median household income by zip code, Carlson Comorbidity Index (CCI), hospital location, bed-size, and teaching status using multivariate regression analysis. Statistical significance was set at a p-value < 0.05. Results In 2019, a total of 39,110 hospitalizations involved patients with SIADH as the reason for the admission and 7.7% of these admissions had comorbid obesity. A higher proportion of hospitalizations involved females, with more of the obese cohort being females (65.7 vs 61.4%, p=0.034). Patients with obesity comparatively had a lower mean age (67.9±13.1 vs 73±13.3 years, p<0.001), a higher proportion of CCI >2, and a higher proportion of Whites. In patients with SIADH, obesity was associated with no difference in mortality (1.1 vs 1.3%, p=0.589) or THC, but patients with obesity had higher odds of increased LOS (5.6 vs 4.9 days, p=0.007), AKI (20 vs 11.3%, aOR: 1.88, p<0.001), and ARF (11.2 vs 7%, aOR: 1.53, p=0.003). There was no significant difference in CVA, PE, septic shock or AMI odds. Conclusions Comorbid obesity was associated with higher LOS and odds of AKI and ARF, but there was no difference in mortality, THC, CVA, PE, septic shock or AMI compared to SIADH hospitalizations without obesity. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.

ODP316 Hyponatremia as a Prognostic Factor for Mortality in COVID-19 at The National Hospital "Dos de Mayo", Lima Peru.

Abstract Introduction Hyponatremia is the most common electrolyte disorder in hospitalized patients. It's more common in patients who were hospitalized with a diagnosed of pneumonia, which worsen the prognosis of the general condition. The infection in patients with SARS-CoV-2, can present hyponatremia, which would affect in a negativity way the recovery of them with mild, moderate or severe respiratory symptoms. Objective Establish if hyponatremia is a prognostic factor of mortality in patients with covid-19 diagnosis.Material and methods: The sample consisted of 185 medical records of patients with a COVID-19 diagnosis, which has been seen between June 2020 and February 2021 an observational, cohort and retrospective study. We recorded epidemiological, demographic, clinical, biochemical and radiological variables of SARS-CoV-2 infection and hyponatremia at the time of diagnosis during hospitalization. Descriptive analysis was used for main variables, Chi square tests, OR calculation and confidence interval were used to assess the statistical association of the variables. Finally, a logistic regression analysis was performed to evaluate confusing variables. Results 160 patients have hyponatremia (34.9% mild, 26.7% moderate and 40% severe) and none of them had a previous diagnosis of SIHAD (Syndrome of inappropriate antidiuretic hormone secretion) consigned in their clinical histories. The increase of mortality was consigned (viewed) in patients with severe hyponatremia compared with moderate and mild hyponatremia diagnosed at hospital admission (20.8% mild hyponatremia, 21.6% moderate and 46.4% severe, p=0. 03) Conclusion Severe hyponatremia at hospital admission was associated with elevated mortality in SARSCoV-2 patients. Presentation: No date and time listed

PMON63 The Impact of Protein-Energy Malnutrition on Outcomes of Adult Hospitalizations for SIADH: A Nationwide Analysis

Abstract Introduction Protein-energy malnutrition (PEM) is a leading cause of morbidity and mortality, particularly in developing countries. Via multiple mechanisms, there is an association between PEM and hyponatremia, but not much is known about concomitant PEM and the syndrome of inappropriate anti-diuretic hormone secretion (SIADH) or the effect of PEM on the outcomes of patients admitted with SIADH. Methods We extracted data from the US Nationwide Inpatient Sample (NIS) for 2019. The NIS contains hospital discharge information estimating yearly US hospitalizations. We included hospitalizations with a principal discharge diagnostic code for SIADH using the ICD-10-CM code (E22.2). Hospitalizations of patients less than 18 years of age were excluded from the study. This cohort was divided based on the secondary diagnosis of PEM. Outcomes analyzed included comparing inpatient mortality rates, mean length of hospital stay (LOS), mean hospitalization cost (THC), and rates of septic shock, acute myocardial infarction (AMI), acute respiratory failure (ARF), acute renal failure (AKI), acute pulmonary edema (PE) between the subgroups. Adjustments were made for age, sex, race, primary payer, median household income by zip code, Charlson Comorbidity Index (CCI), hospital location, bed-size, and teaching status using multivariate regression analysis. Statistical significance was set at a p-value < 0.05. Results There were 39,110 hospitalizations involving patients with SIADH as the reason for the admission in 2019, and 13.2% of them had comorbid PEM. While both cohorts had a higher proportion of females, the subgroup with comorbid PEM had a lower proportion of females comparatively (57.8 vs 62.3%, p=0.006). There was no significant difference in mean age (72.7±13.6 vs 72.1±12.2 years, p=0.113), but the cohort with PEM had a higher proportion of CCI >2 and more ethnic minorities. In patients with SIADH, PEM was associated with higher adjusted odds ratio (aOR) for mortality (2.53 vs 0.9%, aOR: 2.1, p=0.004), increased LOS (6.6 vs 4.7 days, p<0.001) increased THC (13,884 vs 10,223 US$, p <0.001), and higher odds of comorbid septic shock (8.7 vs 2.8%, aOR: 2.69, p=0.014), CVA (14.6 vs 6.5%, aOR: 2.02, p=0.042), PE (8.7 vs 2.5%, aOR: 2.8, p=0.023) and ARF (13 vs 6.5%, aOR: 1.97, p<0.001), with no significant difference in AKI or AMI odds. Conclusions Comorbid PEM was associated with increased odds of mortality, LOS, THC, septic shock, CVA, PE, and ARF in hospitalizations for SIADH. The mechanism of this association is unclear, but further studies are necessary to better understand this potentially important relationship. Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30 p.m.

Endocrine Disorders in Children with Brain Tumors: At Diagnosis, after Surgery, Radiotherapy and Chemotherapy.

Brain tumors are the second most frequent type of all pediatric malignancies. Depending on their localization, patients with brain tumors may present neurological or ophthalmological symptoms, but also weight anomalies and endocrine disorders ranging from growth hormone deficiency, anomalies of puberty, diabetes insipidus to panhypopituitarism. Immediately at diagnosis, all patients with brain tumors require a complete assessment of the hypothalamic-pituitary function in order to address eventual endocrine disorders. Moreover, children and adolescents undergoing brain surgery must receive peri- and postoperative hydrocortisone stress therapy. Post-operative disorders of water homeostasis are frequent, ranging from transient diabetes insipidus, as well as syndrome of inappropriate antidiuretic hormone secretion to persistent diabetes insipidus. Late endocrine disorders may result from surgery near or within the hypothalamic-pituitary region. Pituitary deficits are frequent after radiotherapy, especially growth hormone deficiency. Thyroid nodules or secondary thyroid cancers may arise years after radiotherapy. Gonadal dysfunction is frequent after chemotherapy especially with alkylating agents. Early detection and treatment of specific endocrine disorders at diagnosis, perioperatively, and during long-term follow-up result in improved general and metabolic health and quality of life.

A 43-Day-Old Male With Respiratory Distress and Acute-Onset Hypotonia.

A 43-day-old, full-term, previously healthy male presented with decreased activity and oral intake. He was found to be grunting and hypoxemic on examination, and a respiratory pathogen panel was positive for rhinovirus. He was diagnosed with presumed bronchiolitis. His neurologic exam on admission was normal. Because of respiratory failure, he was escalated from high-flow nasal cannula to bilevel positive airway pressure upon admission and he was started on ceftriaxone and vancomycin while awaiting culture data. On hospital day 6, he required escalation of respiratory support. His examination at that time was notable for new hypotonia of his bilateral upper and lower extremities, sluggish pupils, bilateral exotropia, intermittent vertical nystagmus, and an absent Moro reflex. He developed a focal seizure and a computed tomography of the brain demonstrated simple right otomastoiditis. The seizure was attributed to a serum sodium of 113 mmol/L in the setting of syndrome of inappropriate antidiuretic hormone secretion, thought to be secondary to viral bronchiolitis. However, as the patient's sodium was corrected to a normal range, he continued to have neurologic deficits on examination. Given his persistent hypotonia and respiratory failure, atypical for the expected course of viral bronchiolitis, the patient underwent an extensive neurologic and infectious workup, which ultimately revealed a surprising diagnosis.