A hyponatremic patient with the syndrome of inappropriate antidiuresis (SIAD) gets normal saline (NS), and the plasma sodium decreases, paradoxically. To explain, desalination is often invoked: if urine is more concentrated than NS, the fluid's salts are excreted while some water is reabsorbed, exacerbating hyponatremia. But comparing concentrations can be deceiving. They should be converted to quantities because mass balance is key to unlocking the paradox. The [sodium] equation can legitimately be used to track all of the sodium, potassium, and water entering and leaving the body. Each input or output "module" can be counterbalanced by a chosen iv fluid so that the plasma sodium stays stable. This equipoise is expressed in terms of the iv fluid's infusion rate, an easy calculation called the ratio profile. Knowing the infusion rate that maintains steady state, we can prescribe the iv fluid at a faster rate in order to raise the plasma sodium. Rates less than the ratio profile may risk a paradox, which essentially is caused by an iv fluid underdosing. Selecting an iv fluid that is more concentrated than urine is not enough to prevent paradoxes; even 3% saline can be underdosed. Drinking water adds to the ratio profile and is underestimated in its ability to provoke a paradox. In conclusion, the quantitative approach demystifies the paradoxical worsening of hyponatremia in SIAD and offers a prescriptive guide to keep the paradox from happening. The ratio profile method is objective and quickly deployable on rounds, where it may change patient management for the better.

The diagnosis of Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) relies on an adequate assessment of a hyponatremic state (that is a serum sodium level <136 mmol/l) and on the exclusion of other causative conditions leading to an adequate secretion of antidiuretic hormone (ADH). The understanding of mechanisms involved in pathological ADH secretion is essential for diagnosis and therapy. Although some forms are due to dysregulation in central nervous system regulations, other forms are dependent on diseases in peripheral organs and structures including ADH-producing/secreting neuroendocrine tumors, while others are induced by medical compounds. ADH regulation is closely linked to other systems such as the sympathetic tone, baroreflex regulation. Patients with hyponatremia should be carefully clinically (neurological symptoms) assessed and be classified according to volume status, also with respect for the need of intensive care monitoring. In parallel, laboratory findings of blood and urine must be analyzed appropriately. It is important to demonstrate true hyponatremia, which is paralleled by a decrease in serum osmolality. Mandatory laboratory diagnostic steps comprise the determination of blood and urine electrolytes and serum and urine osmolality, analysis of thyroid, adrenocortical, and kidney function as well as uric acid. Different test results such as a high fractional uric acid excretion may hint to an existing SIADH. Assessment of urine osmolality and urine sodium / potassium concentrations in view of kidney disorders, diuretic use and intravasal volume level allow for further discrimination and may be indicative for a specific underlying disease, covering SIADH. Brain volume changes (“hydrocephalus ex vacuo”) may depend on age rendering the elderly more tolerant to acute or chronic serum sodium changes. The course of an incident hyponatremia, if documented, may affect therapy. A serum sodium drop within less than 48 hours is considered as acute hyponatremia. A rapid bolus of 100 to 150 ml of intravenous 3% hypertonic saline is appropriate to avoid catastrophic outcomes in severe cases of acute symptomatic hyponatremia.

The differential diagnosis of acute stroke is often a challenge for the emergency care staff. In medical literature, about 30% of patients presenting in an emergency department with suspected stroke at initial assessment are actually stroke mimic. We report here a case of a 61-year-old woman who got admitted at the emergency service for an acute stroke that was actually a symptomatic hyponatremia due to a Schwartz-Bartter syndrome associated with an undiagnosed breast cancer. It is very important to quickly identify and manage patients presenting with a high probability of acute stroke even though many other pathological conditions can present with the same clinical onset. Electrolyte disturbances are one of those stroke mimic conditions that are usually reversible if properly identified and treated on time.

Long-term neurocognitive deficits after human herpesvirus-6 (HHV-6) infection are common in stem-cell transplant recipients, but SIADH (Syndrome of inappropriate antidiuretic hormone secretion) with persistent hyponatremia is rare. A 51-year-old woman presented with somnolence, hyponatremia (121 mmol/L) and HHV-6 viremia (80,330 copies/ml) on day +22 post umbilical cord blood transplant (UCBT). With waterrestriction, tolvaptan and combination of foscarnet and ganciclovir, patient's hyponatremia and HHV-6 viremia improved. On day +94 UCBT, hyponatremia and HHV-6 viremia recurred. Foscarnet was restarted and continued until day +269 UCBT due to multiple HHV-6 recurrences with persistent hyponatremia. At day +712, patient remains on water-restriction, tolvaptan for continuous hyponatremia from SIADH.

Transsphenoidal surgery is the first-line treatment for many clinically significant pituitary tumors and sellar lesions. Although complication rates are low when performed at high-volume centers, disorders of salt and water balance are relatively common postoperatively. Both, or either, central diabetes insipidus (recently renamed arginine vasopressin deficiency - AVP-D), caused by a deficiency in production and/or secretion of arginine vasopressin, and hyponatremia, most commonly secondary to the syndrome of inappropriate antidiuresis, may occur. These conditions can extend hospital stay and increase the risk of readmission. This article discusses common presentations of salt and water balance disorders following pituitary surgery, the pathophysiology of these conditions, and their diagnosis and management.

Dysnatremia is a common occurrence in patients with COVID-19 and is associated with higher mortality and risk for septic conditions. The pathomechanisms are probably multifaceted, but severe hyponatremia may also occur as a result of underlying SIADH or hypocortisolism. Patients with preexisting AVP dysfunction, like SIADH or diabetes insipidus, are at high risk for severe electrolyte imbalances in the event of a COVID-19 infection.The recently growing use of immune checkpoint inhibitors in oncology is associated with a spectrum of endocrine immune-related adverse events (endocrine irAEs). These AEs usually occur unpredictably and may even manifest after discontinuation of the anticancer therapy. Hyponatremia is a common factor of several endocrine irAEs and may serve as a red flag biomarker for possibly underlying endocrine irAEs such as hypophysitis or adrenalitis. New-onset hyponatremia should always prompt a comprehensive diagnostic workup and exclusion of endocrine irAEs before the diagnosis of SIADH is made.Hyponatremia with severe symptoms should be treated with hypertonic (3 %) saline solution to resolve the cerebral edema and prevent from detrimental neurological sequelae. Both rapid intermittent bolus (RIB) therapy and continuous infusion therapy have now been reported to be safe and equally effective. The RIB therapy limits the risk of overcorrection and requires less often re-lowering treatment than continuous infusion therapy.Fluid restriction has long been considered as first-line treatment of chronic hyponatremia due to SIADH. Additional treatment with Furosemid and/or oral NaCl tablets does not improve efficacy but reduces tolerance to therapy.Copeptin-based dynamic tests show higher diagnostic accuracy in the differential diagnosis of patients with hypotonic polyuria polydipsia syndrome than the indirect water deprivation test.

A novel rapid spreading and changing virus called SARS-CoV-2 appeared in Wuhan city in December 2019. It was announced by the World Health Organization (WHO) as a pandemic disease in March 2020. It commonly presents with respiratory symptoms; however, it may be asymptomatic. Electrolyte abnormalities are not uncommon features of SARS-CoV-2 infection. Hyponatremia is one of these electrolyte disturbances among SARS-CoV-2 patients, and it may produce symptoms such as weakness and seizure as the initial presenting symptoms. The underlying mechanism(s) of hyponatremia due to SARS-CoV-2 infection is (are) not established. The aim of this review is to evaluate the possible mechanism of hyponatremia in patients with COVID-19. Understanding and categorizing the hyponatremia in these patients will lead to better treatment and correction of the hyponatremia. A review of the literature between December 2019 and March 2022 was conducted searching for the possible reported mechanism(s) of hyponatremia in SARS-CoV-2. Although SIADH is the commonly reported cause of hyponatremia in SARS-CoV-2 infection, other causes such as diarrhea, vomiting, and kidney salt loss must be considered before SIADH.

Eosinophilic granulomatosis with polyangiitis (EGPA, Churg-Strauss syndrome) is a rare multisystem necrotizing vasculitis that involves small- to medium-sized blood vessels. We report a rare case of syndrome of the inappropriate antidiuretic hormone (ADH) secretion (SIADH) secondary to EGPA. A 53-year-old man applied with complaints of pain in the large joints and morning stiffness in knee for 2 months. The patient had the history of impaired fasting glucose, asthma, nasal polyps, and urticaria. Physical examination revealed intrinsic muscle atrophy and weakness in the right hand. Peripheral eosinophil count was 9.78 × 109/L (0.02-0.5), erythrocyte sedimentation rate 39 mm/h (0-20), and C-reactive protein 5.77 mg/dL (0-0.5). Migratory ground-glass pulmonary opacities had been reported in previous chest computed tomography scans. Echocardiography revealed findings compatible with eosinophilic involvement. Electroneuromyographic evaluation showed acute distal axonal neuropathy of right ulnar nerve. EGPA was considered. Oral methylprednisolone treatment was initiated. Intravenous immunoglobulin (IVIG) and cyclophosphamide treatment and gradual tapering of oral steroids were planned. In 24-h urine analysis, sodium was 387 mEq, creatinine was 1156 mg, and volume was 3000 mL. When his medical records were investigated, it was observed that hyponatremia was present for nearly 2 years. While serum osmolality was 270, urine osmolality was 604 mOsm/kg H2O. So, SIADH diagnosis was made. Fluid intake was restricted. Although the patient's sodium level did not return to normal, it rose up to 130 mEq/L. After second cycle of EGPA treatment (cyclophosphamide and IVIG), serum sodium was normal. There is only four other documented cases of SIADH associated with EGPA. We hypothesized that blood supply to the hypothalamus and/or posterior hypophysis might be affected from EGPA vasculitis. Here, in this case, with effective treatment of EGPA, SIADH was resolved which implies a causality between two conditions.

Hyponatremia, defined as a serum sodium <135 mmol/L, is frequently encountered in patients presenting to the emergency department. Symptoms are often unspecific and include a recent history of falls, weakness and vertigo. Common causes of hyponatremia include diuretics, heart failure as well as Syndrome of Inappropriate Antidiuresis (SIAD) and correct diagnosis can be challenging. Emergency treatment of hyponatremia should be guided by presence of symptoms and focus on distinguishing between acute and chronic hyponatremia.

Adverse events, particularly severe adverse events, after coronavirus disease vaccination are the primary concern for many patients. We present the first report of symptomatic hyponatremia, a potentially life-threatening condition, after administration of the ChAdOx1 nCoV-19 coronavirus disease-19 vaccine. A 24-year-old man developed altered consciousness and high-grade fever a day after receiving this vaccine. Computed tomography of the brain showed diffuse brain swelling with bilateral descending transtentorial brain herniation. His serum sodium level, urine sodium level, and urine osmolarity were 114 mEq/L, 77 mEq/L, and 230 mOsm/kg, respectively. He was diagnosed with symptomatic hyponatremia due to syndrome of inappropriate antidiuretic hormone. His symptoms rapidly improved after treatment with 3% NaCl. Seven days after admission, his serum sodium level was normal, and no further intervention was required. We believe that the vaccine was the trigger for hyponatremia in this case based on temporal relationship of vaccination and hyponatremia, the rapid improvement of the patient, and the transient nature of the hyponatremia. We postulate that cytokine underlies the pathophysiology of hyponatremia in this case. Recognition of adverse events after coronavirus disease-19 vaccination is essential. Symptomatic hyponatremia should be included in the differential diagnosis in altered-consciousness patients after administration of ChAdOx1 nCoV-19 coronavirus disease-19 vaccine.

The neurohypophysis (pars posterior) is a structure that is located at the base of the brain and is the posterior lobe of the pituitary gland. Its embryological origin is from the neuroectodermal layer called the infundibulum. The neurohypophysis is divided into two regions; the pars nervosa and the infundibular stalk. Sometimes the pars intermedia and the median eminence are included. It secretes oxytocin and vasopressin; vasopressin is also called antidiuretic hormone (ADH) due to its function of preventing diuresis. These hormones are produced at the magnocellular neurosecretory cells in the hypothalamus, specifically, from the paraventricular nuclei and supraoptic nuclei of the hypothalamus. These cells are neurons that project axons to the neurohypophysis. The hormones are transported from the hypothalamus to the neurohypophysis where they are stored and later released into the neurohypophyseal capillaries, which then carry the hormones into the systemic circulation.[1] Dysfunction of the posterior pituitary affects the hormonal homeostasis, which causes diabetes insipidus (DI), and the syndrome of inappropriate antidiuretic hormone (SIADH) secretion. Disorders caused by oxytocin deficiency are rare, but most are related to pregnancy and lactation problems. The posterior pituitary contains pituicytes that function in the pars nervosa like glial cells for support and modulation of the release of the hormones. A  tumor formed from the pituicytes is called pituicytoma.

The aim of this work is to examine our experience in the use of urea in patients with SIADH. Observational retrospective analysis of 48 patients with SIADH that have been treated with urea in a third-level hospital. Pre-post analysis of serum sodium levels. The 48 patients with SIADH had a median age of 78.5 (range 26-97 years). The serum sodium nadir was 119.8 ± 5.0 mmoL/L and at the beginning of treatment 125.6 ± 4.1 mmoL/L. The patients continued the treatment for a mean time of 2.95 ± 6.29 months, being the treatment still active in 4 patients. In all patients there was an improvement in serum sodium, being the final serum sodium at the end of treatment 134.4 ± 4.9 mmoL/L (p < 0.01). This improvement was observed from the first week. Adverse events were only detected in 2 patients with mild digestive symptomatology and 2 patients refused the treatment due to the low palatability of the urea. There was an economic cost reduction of 87.9% in comparison with treatment with tolvaptan. Urea has shown to be a safe and cost-effective option for the treatment of hyponatremia caused by SIADH.

A 9-year-old girl with remarkable hyponatremia was diagnosed with SIADH that was likely secondary to varicella. Under appropriate treatment, her serum sodium returned to the normal level. There was no evidence of hyponatremia at a 3-month follow-up. We propose that medical professionals need to consider the existence of that SIADH when treating patients with varicella who present with severe hyponatremia.

Hyponatremia is the most frequent electrolytic disorder in hospitalized patients, and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), the most frequent cause of hiponatremia with clinically normal extracellular volume. It consists of a disorder of the regulation of body water that obeys to different causes, mainly cancer, pulmonary illnesses, disorders of the central nervous system and diverse drugs. As in any hiponatremia it a physiological knowledge of the regulation of body water and sodium is essential as well as the application of precise diagnostic criteria in order to manage the problem with an effective treatment. The available data until the moment show that the clinical diagnosis of SIADH made by professionals is mainly not supported on the established criteria drawn by experts and this lack of accuracy probably hits in the therapeutic result. The basis of the treatment of the SIADH is to correct its cause, water restriction, solutes (sodium chloride) and the use of vaptans in case of failure of the previous measures.

Ayahuasca is a psychedelic blend originating from South America that has been used for hundreds of years by local tribes in ritualistic ceremonies. For the last few decades, its usage has expanded to North America in various mindfulness retreats that can benefit from its hallucinogenic properties. In this case report, our patient had attended a satanic ritual where he had consumed copious amounts of Ayahuasca over three days. Upon his return, he continued having demonic hallucinations along with paranoid delusion with increasing bouts of nausea and vomiting. He was brought in by first responders due to suicidal ideations, and shortly after arrival, he became unresponsive with seizure-like activity. The patient was evaluated to be comatose with a Glasgow Coma Scale (GCS) score of 3, and upon securing the airway, was transferred to the critical care unit. Laboratory results showed a case of hypoosmolar hyponatremia secondary to syndrome of inappropriate antidiuretic hormone secretion (SIADH), and following the supportive care, he was able to recover within four days of admission. We theorize that due to the similarity in the pharmacodynamics of the active compound of Ayahuasca, and drugs such as monoamine oxidase inhibitors (MAOI) and 3,4-methylenedioxymethamphetamine (MDMA), it can result in SIADH in its users.

Syndrome of inappropriate anti-diuretic hormone release (SIDAH) is a condition characterized by an unregulated release of anti-diuretic hormone (ADH) resulting in increased water retention and decreased plasma osmolarity. Without regulation, ADH release will cause a significant decrease in plasma sodium concentration and can present with cramping, nausea, vomiting, and in severe cases, seizures, and potentially falling into a comatose state. The causes of SIADH are variable and range from infections, some malignancies to some medications. We report a rare case of SIADH resulting from a single cycle of doxorubicin and cyclophosphamide chemotherapy in a 66-year-old female with left and right, estrogen receptor positive breast cancer who experienced seizures resulting from a dramatic drop in sodium levels.