Case Report: A case of thoracoscopic mediastinal tumor resection in a child with ROHHAD syndrome.

Rapid-onset obesity with hypoventilation, hypothalamic dysfunction, and autonomic dysregulation (ROHHAD) is an exceptionally rare condition. This case report highlights a child diagnosed with ROHHAD syndrome, presenting with a mediastinal tumor. ROHHAD syndrome is characterized by early onset obesity, hypothalamic dysfunction, autonomic dysfunction, inadequate ventilation, suspected seizures, and abnormal behavior. The presence of a mediastinal tumor necessitated surgical intervention. Key considerations during surgery included hypernatremia due to hypothalamic dysfunction, potential airway challenges, preoperative anemia, and hemodynamic fluctuations during the removal of the sizable mediastinal tumor. Comprehensive preparations ensured a safe operation. Notably, some children with this syndrome may exhibit symptoms such as decreased gastrointestinal function, polyuria, and thermoregulatory disturbances. Vigilance is essential during anesthesia assessment in these patients. Anesthesiologists should enhance their knowledge of this condition and tailor their management strategies based on individual clinical presentations and the specific planned surgical procedures.

Effects of donors' and recipients' preoperative serum sodium on the prognosis of liver transplantation.

Dysnatremia is common in donors and recipients of liver transplantation (LT). However, the influence of dysnatremia on LT prognosis remains controversial. This study aimed to investigate effects of donors' and recipients' serum sodium on LT prognosis. We retrospectively reviewed 248 recipients who underwent orthotopic LT at our center between January 2016 and December 2018. Donors and recipients perioperative and 3-year postoperative clinical data were included. Delta serum sodium was defined as the donors' serum sodium minus the paired recipients' serum sodium. Donors with serum sodium > 145 mmol/L had significantly higher preoperative blood urea nitrogen (BUN) (P < 0.01) and creatinine (Cr) (P < 0.01) than others. Preoperative total bilirubin (TBIL) (P < 0.01), direct bilirubin (DBIL) (P < 0.01), BUN (P < 0.01), Cr (P < 0.01) were significantly higher in the hyponatremia group of recipients than the other groups, but both of donors' and recipients' serum sodium had no effect on the LT prognosis. In the delta serum sodium < 0 mmol/L group, TBIL (P < 0.01) and DBIL (P < 0.01) were significantly higher in postoperative 1 week than the other groups, but delta serum sodium had no effect on the postoperative survival rates. Dysnatremia in donors and recipients of LT have no effect on postoperative survival rates, hepatic and renal function, but recipients with higher serum sodium than donors have significantly higher TBIL and DBIL at 1 week postoperatively.

Poisoning with table salt while treating drug poisoning.

Hypernatremia is an increase in serum sodium concentration above 145 mmol/L. There are many causes of elevated sodium levels in the blood serum. One is incorrect actions performed by medical staff. The symptoms of excessively high serum sodium levels depend on the severity of hypernatremia, the rate of its increase and the accompanying volume disorders. Severe symptoms include altered consciousness, increased muscle tone and reflexes, convulsions, psychomotor hyperactivity or drowsiness (up to coma), respiratory failure, and even death. We present the case of a 45-year-old man who took seven tablets of a blood pressure-lowering drug, and paramedics subsequently administered a concentrated solution of table salt to induce vomiting. However, vomiting did not occur, leading to hypernatremia. Ultimately, the man survived but developed persistent cognitive dysfunction, including disordered short-term memory and encoding and retrieval of information from long-term memory, weakening of attention function and fatigue, and disorders in abstract thinking. The patient's family went to the prosecutor's office to investigate the possibility of medical malpractice. Experts found that the paramedics' actions were incorrect. Although it has been known for many years that table salt solutions should not be used to induce vomiting, unfortunately, both laypeople and medical professionals are still using this technique. Iatrogenic salt poisoning may end not only in serious health complications but also in legal consequences.

Evaluation of Maternal Risk Factors for Neonatal Hypernatremic Dehydration: A Systematic Review.

BACKGROUND: Neonatal hypernatremic dehydration (NHD) is a severe condition associated with neonatal morbidity and mortality. PURPOSE: The present study evaluated maternal risk factors, including duration of maternal hospitalisation, primiparity, caesarean section, and pregnancy complications, as well as social factors, such as depression, fatigue, and inadequate support for NHD. DATA SOURCES: PubMed, Cochrane Library, International Scientific Indexing, Scopus, and Google Scholar were the databases searched until 2023. STUDY SELECTION: Articles written in English or Persian focusing on the relationship between maternal risk factors and NHD among neonates and providing sufficient information on NHD were included in this study. On the other hand, articles whose abstracts were only available were excluded. DATA EXTRACTION: The extracted data were presented in Excel software with the following titles: authors' names, year, type of study, study location, and maternal risk factors. The methodological quality of the articles was determined using the quality assurance tool for the diagnostic accuracy score (QUADAS). RESULTS: Of the 58 searched articles, 16 were investigated, which included five prospective, seven cross-sectional, and four retrospective articles. Maternal risk factors for NHD included labour and delivery complications, childbirth complications, factors causing insufficient breast milk intake (including breast milk insufficiency, nipple problems, wrong breastfeeding techniques, breast disorders, types of feeding, and breastfeeding training/counselling in pregnancy), as well as delivery and the postpartum period. IMPLICATIONS FOR PRACTICE AND RESEARCH: Maternal problems in pregnancy and delivery, breast disorders, breastfeeding status, maternal knowledge, and lactation skills are the most common maternal risk factors for NHD. Timely (antenatal) identification and proper management of maternal risk factors help reduce the incidence and severity of NHD complications.

Prediction of plasma sodium changes in the acutely ill patients: the potential role of tissue sodium content.

BACKGROUND: Rapid correction of dysnatremias can result in neurological complications. Therefore, various formulas are available to predict changes in plasma sodium concentration ([Na+]) after treatment, but these have been shown to be inaccurate. This could be explained by sodium acumulation in skin and muscle tissue, which is not explicitly considered in these formulas. We assessed the association between clinical and biochemical factors related to tissue sodium accumulation and the discrepancy between predicted and measured plasma [Na+]. METHODS: We used data from an intensive care unit (ICU) cohort with complete data on sodium, potassium, and water balance. The predicted plasma [Na+] was calculated using the Barsoum-Levine (BL) and the Nguyen-Kurtz (NK) formula. We calculated the discrepancy between predicted and measured plasma sodium and fitted a linear mixed-effect model to investigate its association with factors related to tissue sodium accumulation. RESULTS: We included 594 ICU days of sixty-three patients in our analysis. The mean plasma [Na+] at baseline was 147±6 mmol/L. The median (IQR) discrepancy between predicted and measured plasma [Na+] was 3.14 mmol/L (1.48, 5.55) and 3.53 mmol/L (1.81, 6.44) for the BL and NK formulas, respectively. For both formulas, estimated total body water (p=0.027), initial plasma [Na+] (p<0.001) and plasma [Na+] change (p<0.001) were associated with the discrepancy between predicted and measured plasma [Na+]. CONCLUSION: In this ICU cohort, initial plasma [Na+], total body water, and plasma [Na+] changes, all factors that are related to tissue sodium accumulation, were associated with the inaccurateness of plasma [Na+] prediction.

Challenges in Diagnosing and Managing Severe Hypernatremia in Patients With Major Depressive Disorder: A Case Report.

Hypernatremia, characterized by a plasma sodium concentration above 145 mmol/L, is frequently observed in critically ill patients, often due to factors such as gastrointestinal losses, dehydration, and diabetes insipidus. Psychiatric patients, particularly those with major depressive disorder, are also at risk of developing hypernatremia due to abnormalities in thirst sensation, mineralocorticoid excess, or medication side effects. Severe hypernatremia in psychiatric patients is associated with a high mortality rate, presenting challenges in diagnosis and management. The treatment of chronic hypernatremia (>48 hours) typically involves administering isotonic saline to hypovolemic patients until normalization of vital signs, followed by dextrose 5% in water (D5W) based on water deficit and losses. The goal is to decrease plasma sodium by 8-10 mmol/day. Acute hypernatremia (<48 hours) is corrected with a plasma sodium reduction of 1 mmol/L/hour in the first six to eight hours. While there are no clear guidelines for sodium correction in severe hypernatremia, the literature suggests a safe correction rate of 8-10 mmol/day for chronic hypernatremia and 1 mmol/L/hour for acute cases. In a specific case, a 51-year-old female with severe depression and reduced oral intake was admitted. She exhibited signs of dehydration and was found to have severe hypernatremia (191 mmol/L) with acute kidney injury. Treatment involved D5W, followed by D5W/half-normal saline at 150 mL/hr. Within 24 hours, her plasma sodium decreased to 178 mmol/L and gradually normalized to 143 mmol/L without neurological complications. This case highlights the challenges and underscores the importance of early recognition and management of severe hypernatremia in psychiatric patients. The primary treatment approach addresses water deficits and losses and administers D5W. Recent findings suggest that rapid correction of the condition is acceptable.

Electrolyte disorders related emergencies in children.

This article provides a comprehensive overview of electrolyte and water homeostasis in pediatric patients, focusing on some of the common serum electrolyte abnormalities encountered in clinical practice. Understanding pathophysiology, taking a detailed history, performing comprehensive physical examinations, and ordering basic laboratory investigations are essential for the timely proper management of these conditions. We will discuss the pathophysiology, clinical manifestations, diagnostic approaches, and treatment strategies for each electrolyte disorder. This article aims to enhance the clinical approach to pediatric patients with electrolyte imbalance-related emergencies, ultimately improving patient outcomes.Trial registration This manuscript does not include a clinical trial; instead, it provides an updated review of literature.

Takotsubo Cardiomyopathy Complicating Diabetic Ketoacidosis, Hypothermia and Hypernatremia in a Comatose Patient.

Takotsubo cardiomyopathy (TCM) is a transient wall motion abnormality of the left ventricular apex associated with emotional or physical stress. In the setting of diabetic ketoacidosis (DKA), it is thought to be caused by the compound effect of a catecholamine surge and the noxious effect of acidosis and ketones leading to myocardial stunning. In this report, the first of its kind in the Middle East, we describe the case of a 71-year-old comatose patient, who was being treated for DKA and hypernatremia and was incidentally diagnosed with TCM. We also review 15 case reports of DKA-induced TCM published to date in the literature, many of which had an atypical presentation and good outcomes. Furthermore, we discuss possible risk factors for TCM in our case and supporting literature. It is recommended to maintain increased vigilance and attempt early identification of such conditions in acutely ill patients to prevent life-threatening complications.

Adipsic hypernatremia with marked hyperprolactinemia and GH deficiency in a 9-year-old boy.

Adipsic hypernatremia is typically caused by congenital dysplasia of the hypothalamus and pituitary or brain tumors. However, cases of adipsic hypernatremia without underlying organic abnormalities are rare, and some cases have been reported to be complicated by hypothalamic-pituitary dysfunction. The patient in this case was a 9-yr-old boy who was referred to our hospital because of hypernatremia. His growth chart revealed that he had rapidly become obese since infancy, with growth retardation since the age of seven. His hands and feet were very cold, and he had erythema on his abdomen, indicating possible autonomic dysregulation due to hypothalamic dysfunction. Several hormone load tests showed severe GH deficiency (GHD) and marked hyperprolactinemia (peak: 302.8 ng/mL). Magnetic resonance imaging revealed no organic abnormalities in the hypothalamus and pituitary gland. GH replacement therapy was initiated. Although his growth rate improved, obesity persisted. To the best of our knowledge, this is the first report of adipsic hypernatremia without organic intracranial abnormalities that was treated with GH. Moreover, the patient's prolactin levels were higher than those reported in previous studies. In conclusion, adipsic hypernatremia requires the evaluation of pituitary function and appropriate therapeutic interventions.

Hypernatremia in hospitalised adult patients: A protocol for a scoping review.

BACKGROUND: Hypernatremia is a common electrolyte disturbance in hospitalised patients associated with adverse outcomes. The aetiology is diverse but often related to fluid therapy and sodium-containing medicaments. We aim to outline the evidence base on hypernatremia in adult hospitalised patients. METHODS: We will conduct a scoping review and adhere to the preferred reporting items for systematic and meta-analysis extension for scoping reviews (PRISMA-ScR). We will systematically search the Cochrane Library, Medline, Pubmed, and Embase from inception with no limitations to language, and include all study designs. We will use the population, exposure, comparator, and outcome-based approach to define eligibility criteria. The population: adult hospitalised patients; exposure: hypernatremia; comparator: no hypernatremia or all types of treatments of hypernatremia; and outcomes: all reported outcomes. Two authors will independently screen and select studies followed by full-text assessment and data extraction in duplicate. All outcome measures will be reported, and descriptive analyses will be performed. The certainty of evidence will be assessed according to an adapted grading of recommendations assessment, development, and evaluation (GRADE) approach. DISCUSSION: This scoping review will provide an overview of the current evidence regarding the incidence of hypernatremia, treatment modalities, and outcomes reported for hospitalised adult patients with hypernatremia.

Autoimmunity related to anti-Nax and anti-ZSCAN1 autoantibodies in adipsic hypernatremia.

"Adipsic hypernatremia" is clinically characterized by chronic elevation of plasma [Na+] with an inappropriate lack of thirst and upward resetting of the osmotic set point for arginine vasopressin (AVP) secretion, combined with a relative deficiency of AVP, thereby resulting in persistent hypernatremia. Many cases are accompanied by structural lesions in the hypothalamus, pituitary gland, and circumventricular organs (CVOs). On the other hand, cases without structural lesions have been reported since the 1970s, but the pathophysiology was unknown for a long time. In 2010, Hiyama et al. reported that an anti-Nax antibody response caused adipsic hypernatremia in a pediatric case with ganglioblastoma. In recent years, advances in clinical research have led researchers to recognize that an autoimmunological pathogenic mechanism might be associated with periventricular organs such as the subfornical organ (SFO). In addition, in pediatric cases diagnosed as ROHHAD (rapid-onset obesity with hypoventilation, hypothalamic dysfunction, autonomic dysregulation) syndrome, it has been reported that half of the cases have abnormal serum Na levels, and some research findings indicated an autoimmune mechanism acting on the organs of the hypothalamus and CVOs. Then, anti-ZSCAN1 antibody response was detected in cases diagnosed as ROHHAD-NET in 2022. In this review, by summarizing a series of studies on Nax and ZSCAN1, which are expressed in the hypothalamus, pituitary gland, and SFO, I would like to describe the current findings of the autoimmune pathogenesis of adipsic hypernatremia.

Dysnatremia as a Mortality Marker in Intensive Care Patients with SARS-CoV-2 Infection: A Retrospective Study.

Background and Objectives: The Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection may cause acute respiratory failure, but also remains responsible for many other pathologies, including electrolyte disorders. SARS-CoV-2 infection causes disorders in many systems and can disrupt water homeostasis with thirst and appetite abnormalities. Dysnatremia affects prognosis, and may be associated with mortality in patients admitted to an intensive care unit (ICU) diagnosed with SARS-CoV-2. Materials and Methods: The study included 209 patients admitted to the ICU between 12 April 2021 and 1 March 2022 who were over 18 years old and diagnosed with SARS-CoV-2 infection by clinical and thoracic tomography findings or with a positive reverse transcription polymerase chain reaction (RT-PCR) test result. The laboratory markers, treatment modalities, nutritional, and respiratory support also for outcome evaluation, length of stay in the ICU, total hospitalization duration, and mortality in the ICU were recorded. The laboratory marker comparison was made using admission with the final assessment performed before the time of mortality in the ICU or after discharge. Results: Inotropic requirements among patients were high, which reflected mortality in the ICU. Hypernatremia presence was associated with an increase in enteral support, the inotropic support requirement, and mortality. Hypernatremia was correlated with diabetes mellitus, chronic renal failure, and a longer duration under mechanical ventilation. Conclusions: Hypernatremia was an important risk factor in ICU patients hospitalized for SARS-CoV-2 infection, which was also affected by the treatment regimens given themselves. This complex relationship underlies the importance of proper electrolyte management, especially in patients who were under severe stress and organ failure.

Effects of Acute Hypernatremia on the Electrophysiology of Single Human Ventricular Cardiomyocytes: An In Silico Study.

Background: Clinical and experimental data on the cardiac effects of acute hypernatremia are scarce and inconsistent. We aimed to determine and understand the effects of different levels of acute hypernatremia on the human ventricular action potential. Methods: We performed computer simulations using two different, very comprehensive models of the electrical activity of a single human ventricular cardiomyocyte, i.e., the Tomek-Rodriguez model following the O'Hara-Rudy dynamic (ORd) model and the Bartolucci-Passini-Severi model as published in 2020 (known as the ToR-ORd and BPS2020 models, respectively). Mild to extreme levels of hypernatremia were introduced into each model based on experimental data on the effects of hypernatremia on cell volume and individual ion currents. Results: In both models, we observed an increase in the intracellular sodium and potassium concentrations, an increase in the peak amplitude of the intracellular calcium concentration, a hyperpolarization of the resting membrane potential, a prolongation of the action potential, an increase in the maximum upstroke velocity, and an increase in the threshold stimulus current at all levels of hypernatremia and all stimulus rates tested. The magnitude of all of these effects was relatively small in the case of mild to severe hypernatremia but substantial in the case of extreme hypernatremia. The effects on the action potential were related to an increase in the sodium-potassium pump current, an increase in the sodium-calcium exchange current, a decrease in the rapid and slow delayed rectifier potassium currents, and an increase in the fast and late sodium currents. Conclusions: The effects of mild to severe hypernatremia on the electrical activity of human ventricular cardiomyocytes are relatively small. In the case of extreme hypernatremia, the effects are more pronounced, especially regarding the increase in threshold stimulus current.

Transient Diabetes Insipidus After Vasopressin Discontinuation.

Vasopressin infusion is commonly used in intensive care settings during states of advanced vasodilatory shock for its vasoconstrictive properties. Vasopressin also acts on renal tubular cell receptors in the collecting ducts of kidneys to allow for water reabsorption. The sudden discontinuation of vasopressin infusion can lead to the development of transient diabetes insipidus (DI) with classic findings of polyuria, dilute urine, and hypernatremia. We report the case of a 59-year-old male who underwent an emergent bedside cricothyrotomy procedure secondary to papillary carcinoma of the thyroid and subsequently developed septic shock requiring initiation of vasopressin infusion for hemodynamic support. He remained on vasopressin for five days before the infusion was discontinued after clinical improvement. Within 12 hours of vasopressin discontinuation, the patient developed polyuria (> 3 L/day urine output) with volumes as high as 1 L per hour. His serum sodium levels increased more than 10 mmol/L from 137 to 149 mmol/L. This case is unique from prior reports, as our patient was without any neurological or neurosurgical comorbidities that would predispose him to an organic central cause of DI. Furthermore, the patient's large-volume diuresis and serum abnormalities spontaneously self-improved within 24 hours without significant medical intervention. In conclusion, this case adds to a growing number of reports of transient DI following vasopressin withdrawal, demonstrating the need to formally recognize this occurrence as a potential consequence of vasopressin use in intensive care settings.

Effects of hypernatremia on the microglia.

Signs and symptoms of hypernatremia largely indicate central nervous system dysfunction. Acute hypernatremia can cause demyelinating lesions similar to that observed in osmotic demyelination syndrome (ODS). We have previously demonstrated that microglia accumulate in ODS lesions and minocycline protects against ODS by inhibiting microglial activation. However, the direct effect of rapid rise in the sodium concentrations on microglia is largely unknown. In addition, the effect of chronic hypernatremia on microglia also remains elusive. Here, we investigated the effects of acute (6 or 24 h) and chronic (the extracellular sodium concentration was increased gradually for at least 7 days) high sodium concentrations on microglia using the microglial cell line, BV-2. We found that both acute and chronic high sodium concentrations increase NOS2 expression and nitric oxide (NO) production. We also demonstrated that the expression of nuclear factor of activated T-cells-5 (NFAT5) is increased by high sodium concentrations. Furthermore, NFAT5 knockdown suppressed NOS2 expression and NO production. We also demonstrated that high sodium concentrations decreased intracellular Ca2+ concentration and an inhibitor of Na+/Ca2+ exchanger, NCX, suppressed a decrease in intracellular Ca2+ concentrations and NOS2 expression and NO production induced by high sodium concentrations. Furthermore, minocycline inhibited NOS2 expression and NO production induced by high sodium concentrations. These in vitro data suggest that microglial activity in response to high sodium concentrations is regulated by NFAT5 and Ca2+ efflux through NCX and is suppressed by minocycline.

Effect of fosfomycin-induced hypernatremia on patients' hospital stay length and survival.

BACKGROUND AND OBJECTIVE: Hypernatremia is a possible side effect of intravenous fosfomycin. The aim of this study was to investigate the effects of changes in sodium (Na) levels on hospital stay and survival in patients hospitalized in the intensive care unit receiving fosfomycin. SUBJECTS AND METHODS: This study was conducted retrospectively on the files of patients over the age of 60, who were admitted to the Internal Medicine Intensive Care Unit. Plasma sodium levels were observed and documented over a period of 14 days. The patients were divided into two groups (Hypernatremia group Na > 145 mEq/L vs normonatremia group 135-145 mEq/L). In addition, daily sodium changes were noted for 14 days in patients. RESULTS: The mean age of the patients was 75 years. Hospitalization days were longer for hypernatremia patients (31.5 days vs 41 days, p = 0.003). Patients with hypernatremia had an extended duration of stay in the intensive care unit. (21 days vs 31 days p = 0.002). The 1-month survival rate was 61.4% in patients with hypernatremia and 24.9% in patients without hypernatremia (p = 0.004). The absence of hypernatremia increases mortality by 2.09 times (95% CI 1.35-3.23). When discharge and mortality rates were analyzed according to sodium fluctuation, discharged patients exhibited a lower sodium fluctuation (4 min/max (-10/19) vs 6 min/max (-16/32) p < 0.001). CONCLUSION: In conclusion, the strength of our study is that it specifically focuses on the consequences of the sodium fluctuation on patient management and provides results.

Comparison of prognosis between hyperbilirubinemic infants with and without hypernatremia.

OBJECTIVES: Hypernatremia may facilitate the diffusion of bilirubin through the blood-brain barrier and increase the risk of bilirubin encephalopathy. This study was conducted to compare the prognosis of jaundice infants with those with jaundice and hypernatremia. METHODS: A total of 615 term infants with idiopathic jaundice with or without hypernatremia were enrolled in this cohort study with 24-months follow-up at Ghaem Hospital, Mashhad, Iran, between 2010 and 2022. An in-house questionnaire including the laboratory evaluation and neonatal characteristics was used as the data collection tool. The follow-up of neonatal development status was performed using the Denver test II at 6, 12, 18, and 24 months after discharging from hospital. RESULTS: Normal outcomes were seen in 555 (90.2%) out of 615 studied infants, while 60 cases (9.8%) showed abnormal outcomes. Serum levels of sodium (P = 0.017), bilirubin (P = 0.001), urea (P = 0.024), and creatinine (P = 0.011) as well as hyperthermia (P = 0.046) and unconsciousness (P = 0.005) showed significant differences between the two groups. Approximately 16% of the newborns with both jaundice and hypernatremia, and 9% of those with only jaundice had unfavorable prognoses. Also, bilirubin level had the most predictive power (91.3%). CONCLUSIONS: Our results suggest that hypernatremia or jaundice alone, may affect the prognosis of infants aged 2 years; but jaundice and hypernatremia together, will intensify the developmental problems in jaundice infants. However, the role of hyperbilirubinemia in the incidence of complications is more than hypernatremia.

A Case of Hypernatremia in a Newly Diagnosed Patient With Acute Myeloid Leukemia: Lessons for Nephrologists.

Arginine vasopressin deficiency (AVP-D), formerly known as central diabetes insipidus, is a disease characterized by polyuria, polydipsia, and hypernatremia. The concomitant diagnosis of acute myeloid leukemia (AML) is an underappreciated event that requires prompt recognition and treatment by practicing nephrologists and hematologists. This report highlights this importance by describing the case of a 39-year-old patient newly diagnosed with AML who developed severe hypernatremia. The role of diagnostic testing through desmopressin (DDAVP) challenge and copeptin testing to confirm the diagnosis of AVP-D in this context and the use of DDVAP for treatment are discussed. Practicing nephrologists and primary care providers taking care of patients with similar symptoms will benefit from understanding the pathophysiology of AVP-D, its relationship with AML, and the prognosis in this patient cohort.