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.

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.

Acute hypernatremia increases functional connectivity of NaCl sensing regions in the human brain: An fMRI pilot study.

Rodent studies demonstrated specialized sodium chloride (NaCl) sensing neurons in the circumventricular organs, which mediate changes in sympathetic nerve activity, arginine vasopressin, thirst, and blood pressure. However, the neural pathways involved in NaCl sensing in the human brain are incompletely understood. The purpose of this pilot study was to determine if acute hypernatremia alters the functional connectivity of NaCl-sensing regions of the brain in healthy young adults. Resting-state fMRI scans were acquired in 13 participants at baseline and during a 30 min hypertonic saline infusion (HSI). We used a seed-based approach to analyze the data, focusing on the subfornical organ (SFO) and the organum vasculosum of the lamina terminalis (OVLT) as regions of interest (ROIs). Blood chemistry and perceived thirst were assessed pre- and post-infusion. As expected, serum sodium increased from pre- to post-infusion in the HSI group. The primary finding of this pilot study was that the functional connectivity between the SFO and a cluster within the OVLT increased from baseline to the late-phase of the HSI. Bidirectional connectivity changes were found with cortical regions, with some regions showing increased connectivity with sodium-sensing regions while others showed decreased connectivity. Furthermore, the functional connectivity between the SFO and the posterior cingulate cortex (a control ROI) did not change from baseline to the late-phase of the HSI. This finding indicates a distinct response within the NaCl sensing network in the human brain specifically related to acute hypernatremia that will need to be replicated in large-scale studies.

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.

Relationship between sodium level and in-hospital mortality in traumatic brain injury patients of MIMIC IV database.

Background: An association between prognosis and high sodium levels in Traumatic Brain Injury (TBI) patients in Intensive Care Units (ICUs) has been noted, but limited research exists on the ideal sodium level in these patients or the impact on early mortality, using the MIMIC-IV database. Methods: A retrospective survey was conducted on TBI patients from the MIMIC-IV database. Patients were divided into two categories based on their highest serum sodium level within 24 h of admission exceeding 145 mmol/L: those with hypernatremia, and those with moderate-to-low sodium levels. Collected covariates encompasses demographic, clinical, laboratory, and intervention variables. A multivariate logistic regression model was implemented to forecast in-hospital mortality. Results: The study included 1749 TBI patients, with 209 (11.5%) experiencing in-hospital deaths. A non-linear test exposed an L-shaped correlation between sodium level and in-hospital mortality, with mortality rates increasing after a turning point at 144.1 mmol/L. Compared to the moderate-to-low group's 9.3% mortality rate, the hypernatremia group had a significantly higher mortality rate of 25.3% (crude odds ratio = 3.32, 95% confidence interval: 2.37 ~ 4.64, p < 0.001). After adjusting for all covariates, the hypernatremia group continued to show a significant correlation with higher mortality risk (adjusted odds ratio = 2.19, 95% confidence interval: 1.38 ~ 3.47, p = 0.001). This trend remained consistent regardless of the analyses stratification. Conclusion: The study reveals an L-shaped relationship between sodium levels and in-hospital deaths, with a pivotal point at 144.1 mmol/L. TBI patients displaying hypernatremia were independently linked to higher in-hospital mortality, underlining the need for further studies into targeted management of sodium levels in these patients.

Dysnatremia in a changing climate: A global systematic review of the association between serum sodium and ambient temperature.

OBJECTIVE: Both hyponatremia and hypernatremia have been reported to occur more frequently with higher ambient temperatures, although the underlying mechanisms are not well understood. Global temperatures are rising due to climate change, which may impact the incidence of dysnatremia worldwide. We aimed to identify, collate and critically appraise studies analyzing the relationship between climate measures (outdoor temperature, humidity) and serum sodium concentrations. DESIGN: Systematic review, reported in accordance with PRISMA guidelines. METHODS: MEDLINE and Embase were searched with relevant key terms. Studies assessing the effect on serum sodium measurement of elevated temperature or humidity versus a comparator were included. RESULTS: Of 1466 potentially relevant studies, 34 met inclusion criteria, originating from 23 countries spanning all inhabited continents. The majority (30 of 34, 88%) reported a significant association between outdoor temperature and dysnatremia, predominantly lower serum sodium with increased ambient temperature. Humidity had a less consistent effect. Individuals aged above 65 years, children, those taking diuretics and antidepressants, those with chronic renal impairment or those undertaking physical exertion had increased vulnerability to heat-associated dysnatremia. The risk of bias was assessed to be high in all but four studies. CONCLUSIONS: Higher ambient temperature is consistently associated with an increased incidence of hyponatremia. We infer that hyponatremia presentations are likely to rise with increasing global temperatures and the frequency of extreme heat events secondary to climate change. Evidence-based public health messages, clinician education and reduction in fossil fuel consumption are necessary to reduce the expected burden on healthcare services worldwide.

Antibiotics in patients with severe burn injury-A modifiable variable in hypernatremia etiology.

INTRODUCTION: Hypernatremia is a common problem among patients with severe burn injuries and seems to be associated with an unfavorable clinical outcome. The current study was designed to evaluate the impact of antibiotics with a high proportion of sodium on this phenomenon. METHODS: All admissions to our burn center from 01/2017 till 06/2023 were retrospectively screened. All patients aged >18 years which suffered from at least 20 % total body surface burned area (TBSA) 2nd degree burn injuries or more than 10 % TBSA when including areas of 3rd degree burn injuries were included. The course of the serum Na-level was analyzed from two days before till two days after the start of the antibiotic treatment. Ampicillin/sulbactam, cefazoline and piperacillin/tazobactam were classified as high-dose sodium antibiotics (HPS), meropenem and vancomycin as low-dose sodium antibiotics (LPS). RESULTS: 120 patients met the inclusion criteria. A significant increase of the serum Na was detectable in the HPS group on day 1 and 2 after initiating the antibiotic treatment (n = 64, day 1: 2,1 (SD 4,18) mmol/l, p < 0,001; day 2: 2,44 (SD 5,26) mmol/l, p < 0,001) while no significant changes were detectable in the LPS group (n = 21, day 1: 0,18 (SD 7,45) mmol/l, p = 0,91; day 2: -0,27 (SD 7,44) mmol/l, p = 0,87). This effect was further aggravated when analyzing only the HPS patients with a TBSA ≥30 % (n = 33; day 1: 2,93 (SD 4,68) mmol/l, p = 0,002; day 2: 3,41 (SD 5,9) mmol/l, p = 0,003). CONCLUSION: The amount of sodium in antibiotics seems to have a relevant impact on the serum Na during the early stages of severe burn injury. Therefore, this aspect should be taken into account when searching for the most appropriate antibiotic treatment for patients with severe burn injury, especially when being at acute risk for a clinical relevant hypernatremia.

Hypernatremia in Hyperglycemia: Clinical Features and Relationship to Fractional Changes in Body Water and Monovalent Cations during Its Development.

In hyperglycemia, the serum sodium concentration ([Na]S) receives influences from (a) the fluid exit from the intracellular compartment and thirst, which cause [Na]S decreases; (b) osmotic diuresis with sums of the urinary sodium plus potassium concentration lower than the baseline euglycemic [Na]S, which results in a [Na]S increase; and (c), in some cases, gains or losses of fluid, sodium, and potassium through the gastrointestinal tract, the respiratory tract, and the skin. Hyperglycemic patients with hypernatremia have large deficits of body water and usually hypovolemia and develop severe clinical manifestations and significant mortality. To assist with the correction of both the severe dehydration and the hypovolemia, we developed formulas computing the fractional losses of the body water and monovalent cations in hyperglycemia. The formulas estimate varying losses between patients with the same serum glucose concentration ([Glu]S) and [Na]S but with different sums of monovalent cation concentrations in the lost fluids. Among subjects with the same [Glu]S and [Na]S, those with higher monovalent cation concentrations in the fluids lost have higher fractional losses of body water. The sum of the monovalent cation concentrations in the lost fluids should be considered when computing the volume and composition of the fluid replacement for hyperglycemic syndromes.

CARDS, a Novel Prognostic Index for Risk Stratification and In-Hospital Monitoring.

Background: Sodium fluctuation is independently associated with clinical deterioration. We developed and validated a prognostic index based on sodium fluctuation for risk stratification and in-hospital monitoring. Methods: This study included 33,323 adult patients hospitalized at a tertiary care hospital in 2014. The first 28,279 hospitalizations were analyzed to develop the model and then the validity of the model was tested using data from 5044 subsequent hospitalizations. We predict in-hospital mortality using age, comorbidity, range of sodium fluctuation, and duration of sodium fluctuation, abbreviated as CARDS. Results: In-hospital mortality was similar in the derivation (0.6%) and validation (0.4%) cohorts. In the derivation cohort, four independent risk factors for mortality were identified using logistic regression: age (66-75, 2 points; >75, 3 points); Charlson comorbidity index (>2, 5 points); range of sodium fluctuation (7-10, 4 points; >10, 10 points); and duration of fluctuation (≤3, 3 points). The AUC was 0.907 (95% CI: 0.885-0.928) in the derivation cohort and 0.932 (95% CI: 0.895-0.970) in the validation cohort. In the derivation cohort, in-hospital mortality was 0.106% in the low-risk group (0-7 points), 1.076% in the intermediate-risk group (8-14 points), and 8.463% in the high-risk group (15-21 points). In the validation cohort, in-hospital mortality was 0.049% in the low-risk group, 1.064% in the intermediate-risk group, and 8.403% in the high-risk group. Conclusions: These results suggest that patients at low, intermediate, and high risk for in-hospital mortality may be identified by CARDS mainly based on sodium fluctuation.

Excessive sodium supplementation but not fluid load is correlated with overall morbidity in extremely low birth weight infants.

Objectives: Sodium homeostasis in extremely low birth weight (ELBW) infants is critical. While a lack of sodium delays growth, excessive supplementation increases morbidity. Methods: We performed a single-center retrospective study on sodium and fluid management during the first 2 weeks of live including all ELBW infants born between June 1, 2017 and May 31, 2019. Results: Forty-seven patients (median GA 26 + 6 weeks, median BW 845 g) were included. Mean sodium intake was above the ESPGHAN recommendation, 4.58 mmol/kg/day during the first 2 days and 1.99 mmol/kg/day during the following period. Incidence of PDA, IVH, and ROP was directly associated with sodium intake (OR 1.6, 1.3, and 1.4, respectively), but not with fluid supplementation. No association to BPD was found. The most important source for inadvertent sodium intake were 0.9% saline given by arterial lines. Sodium supplementation did not correlate directly with serum sodium levels, but a linear regression model combining sodium intake and fluid supplementation was able to predict serum sodium changes 24-48 h in advance (correlation coefficient of 0.294, p < 0.05). Conclusions: Sodium application substantially exceeded ESPGHAN recommendations in ELBW infants. An excess in sodium was associated with an overall increased morbidity, justifying increased efforts to identify inadvertent sodium sources in these patients with the aim to decrease sodium excess.

Hyperchloremia and Hypernatremia Decreased Microglial and Neuronal Survival during Oxygen-Glucose Deprivation/Reperfusion.

Hyperchloremia and hypernatremia are associated with higher mortality in ischemic stroke, but it remains unclear whether their influence directly contributes to ischemic injury. We investigated the impact of 0.9% sodium chloride (154 mM NaCl), 0.9% sodium acetate (167 mM CH3COONa), and their different combinations (3:1, 2:1, and 1:1) on microglial (HMC-3) and neuronal (differentiated SH-SY5Y) survival during oxygen-glucose deprivation/reperfusion (OGD/R). Further, we assessed the effect of hyperchloremia and hypernatremia-treated and OGD/R-induced HMC-3-conditioned media on differentiated SH-SY5Y cells under OGD/R conditions. We performed cell viability, cell toxicity, and nitric oxide (NO) release assays and studied the alteration in expression of caspase-1 and caspase-3 in different cell lines when exposed to hyperchloremia and hypernatremia. Cell survival was decreased in 0.9% NaCl, 0.9% CH3COONa, combinations of HMC-3 and differentiated SH-SY5Y, and differentiated SH-SY5Y cells challenged with HMC-3-conditioned media under normal and OGD/R conditions. Under OGD/R conditions, differentiated SH-SY5Y cells were less likely to survive exposure to 0.9% NaCl. Expression of caspase-1 and caspase-3 in HMC-3 and differentiated SH-SY5Y cells was altered when exposed to 0.9% NaCl, 0.9% CH3COONa, and their combinations. A total of 0.9% NaCl and 0.9% CH3COONa and their combinations decreased the NO production in HMC-3 cells under normal and OGD/R conditions. Both hypernatremia and hyperchloremia reduced the survival of HMC-3 and differentiated SH-SY5Y cells under OGD/R conditions. Based on the OGD/R in vitro model that mimics human ischemic stroke conditions, it possibly provides a link for the increased death associated with hyperchloremia or hypernatremia in stroke patients.

Hypernatremia and Its Rate of Correction: The Evidence So Far.

Hypernatremia or high serum sodium levels can have many different causes, including insufficient free water intake, or excess free water losses. The management of hypernatremia focuses on resolving the underlying cause, replenishing free water deficit, and preventing further losses while closely monitoring serum sodium concentration. This systematic review was carried out using medical databases such as PubMed, PubMed Central, and Google Scholar for relevant medical literature. The identified articles were reviewed, eligibility criteria were applied, and seven research articles were identified. The effect of the rate of hypernatremia correction on both short- and long-term outcomes in volume-resuscitated patients was the focus of our search for randomized or observational studies. Based on our analysis of the clinical evidence, we concluded that the present recommendations for treating acute and chronic hypernatremia in resuscitated patients do not stem from high-quality research.

Successful Fluid Management in Respiratory Failure due to Clazosentan Following a Cerebral Aneurysm Clipping: A Case Report.

Clazosentan, a potent selective endothelin receptor subtype A antagonist, has been demonstrated to be effective in preventing cerebral vasospasms after subarachnoid hemorrhage. We report the successful management of respiratory failure due to pulmonary edema associated with clazosentan, with a hemodynamic monitoring system. A 49-year-old Japanese man underwent emergency clipping for a right internal carotid-posterior communicating artery aneurysm. The surgery and general anesthesia for the rupture proceeded with no complications. Clazosentan was administered from postoperative day 1 to prevent cerebral vasospasm. He presented with respiratory failure six days post surgery and chest X-ray imaging showed pulmonary edema. In our intensive care unit, the patient's N-terminal pro-brain natriuretic peptide was 476 pg/mL although trans-thoracic echography indicated a normal left ventricular ejection fraction (>60%) and normal diastolic function. The hemodynamic monitoring system showed 11 L/minute cardiac output and a cardiac index of 5.6 L/minute/m2. We thus diagnosed the cause of the patient's respiratory failure as due to excessive volume, as an adverse event of clazosentan. We changed the cerebral vasospasm-preventive drug to fasudil hydrochloride hydrate and forced urination. His body weight dropped approximately 9 kg as of day 9 in the ICU and he was weaned off the ventilator 23 days post surgery. This case indicates the importance of optimal infusion in patients with clazosentan. Optimal fluid management using a hemodynamic monitoring system could be useful for clazosentan-induced respiratory failure.

Antidiuretic hormone deficiency secondary to inactive hydrocephalus: a case report.

BACKGROUND: Diabetes insipidus is a syndrome characterized by polyuria, which is almost always associated with polydipsia. The most frequent cause is central diabetes insipidus, which is the result of an inadequate secretion of the antidiuretic hormone, and diagnosis involves differentiating it from other causes of polyuria and polydipsia. CASE PRESENTATION: Here, we present a clinical case of a previously healthy 13-year-old Nepali boy, who, in December 2022, was found to have intense polydipsia accompanied by polyuria. He had bilateral lower limb weakness at the time of presentation. Biochemical evaluation demonstrated raised serum sodium (181 mEq/L), serum creatinine (78 µmol/L), and serum uric acid (560 µmol/L) with suppressed serum potassium (2.7 mEq/L), which was the major concern to the clinicians. Further laboratory workup revealed an increased serum osmolarity (393.6 mOsm/kg) with reduced urine osmolarity (222.7 mOsm/kg). On contrast magnetic resonance imaging of the brain, a thick-walled third ventricular cyst with bilateral foramen obstruction, thin membrane-like structure at top of aqueduct of Sylvius with gross obstructive hydrocephalus (inactive), and compressed and thinned pituitary gland with no bright spot was observed. The laboratory findings, radiological findings, and case presentation provided the provisional diagnosis of diabetes insipidus due to hydrocephalus and third ventricular cyst. CONCLUSIONS: Central diabetes insipidus due to hydrocephalus, though rare, can have serious complications including the predilection to develop a deficit of other pituitary hormones. Thus, even if hydrocephalus is dormant with normal intracranial pressure, it must be addressed during investigations of central diabetes insipidus.

Persistent hypernatremia secondary to adipsic central diabetes insipidus in a patient with herpes-induced meningoencephalitis and COVID-19 infection: a case report.

Central diabetes insipidus (CDI) typically manifests as a polyuria-polydipsia syndrome, in which normonatremia is generally maintained through the polydipsia. A 53-year-old woman presented with diabetic ketosis and hyperosmolar hyperglycemic syndrome. Her medical history included herpes meningoencephalitis, which was associated with confusion and amnesia. On physical examination, she was apyretic, confused, and had signs of extracellular dehydration. Her capillary glucose concentration was high and her urine was positive for ketones. Laboratory investigations revealed severe hyperglycemia, hypernatremia (plasma hyperosmolarity of 393.6 mOsm/L), and mild acute renal failure. In addition, she had a paucisymptomatic COVID-19 infection. Intravenous rehydration with isotonic saline solution and insulin therapy were effective at controlling the ketosis and ameliorating the hyperglycemia, but failed to normalize the hypernatremia and hyperosmolarity. She was not thirsty and had a urine output of 1 L/day, with urinary hypotonicity. Desmopressin administration reduced the hypernatremia and hyperosmolarity to within their normal ranges, and the patient's urinary osmolarity increased to 743 mOsm/L. Therefore, adipsic CDI was diagnosed. Endocrine investigations revealed isolated central hypothyroidism. The results of pituitary magnetic resonance imaging were normal. Thus, patients with impaired thirst may have an atypical presentation of CDI. In addition, the diagnosis of adipsic CDI is particularly challenging.

Serum sodium level fluctuations following the resection of childhood-onset craniopharyngioma.

BACKGROUND: Craniopharyngiomas are low-grade malignancies (WHO I) in the sellar region. Most cases of childhood-onset craniopharyngioma are adamantinomatous craniopharyngioma, and neurosurgery is the treatment of choice. Affected patients have postoperative complications, including water and electrolyte disturbances, because these malignancies develop near the hypothalamus and pituitary gland. Determining postoperative serum sodium fluctuation patterns in these patients can reduce postoperative mortality and improve prognosis. OBJECTIVE: To measure changes in serum sodium levels in pediatric patients who underwent craniopharyngioma surgery and identify influencing factors. METHODS: This retrospective study measured the serum sodium levels of 202 patients aged 0-18 years who underwent craniopharyngioma resection in Beijing Tiantan Hospital and Beijing Children's Hospital and identified predictors of severe hyponatremia and hypernatremia. RESULTS: The mean age of the cohort was 8.35 ± 4.35 years. The prevalence of hypernatremia, hyponatremia, and their severe forms (serum Na+  > 150 mmol/L and serum Na+  < 130 mmol/L) within 14 days after surgery was 66.3%, 72.8%, 37.1%, and 40.6%, respectively. The mean postoperative serum sodium level showed a triphasic pattern, characterized by two peaks separated by a nadir. Sodium levels peaked on days 2 (143.6 ± 7.6 mmol/L) and 14 (143.2 ± 6.7 mmol/L) and reached their lowest on day 6 (135.5 ± 7.5 mmol/L). A total of 31 (15.3%) patients met the diagnostic threshold for hyponatremia and hypernatremia of the triphase response, whereas 116 (57.4%) patients presented this pattern, regardless of met the diagnostic criteria or not. The prevalence of severe hyponatremia varied depending on preoperative endocrine hormone deficiency, tumor status (primary or recurrent), and surgical approach. CONCLUSIONS: Serum sodium levels after craniopharyngioma resection in children showed a triphasic pattern in most cases. The risk of postoperative hyponatremia varied depending on preoperative endocrine hormone deficiency, tumor status (primary or recurrent), and surgical approach.

Dyselectrolytemia in Children With Severe Pneumonia: A Prospective Study.

Background Pneumonia is a condition characterized by inflammation of the lung parenchyma. It is one of the leading causes of mortality in children below five years of age. While predominantly prevalent in developing countries, it is also associated with significant healthcare-associated costs in developed countries. Among the many risk factors for childhood pneumonia, incomplete immunization, nonexclusive breastfeeding for less than six months, delayed weaning, poor household air quality, malnutrition, and low birth weight are the most commonly found. Electrolyte disturbances, also known as dyselectrolytemia, have been associated with a broad spectrum of acute infections, including pneumonia, particularly hyponatremia. It occurs in the majority of community-acquired pneumonia. Hyper- and hypokalemia are less frequently occurring electrolyte disturbances. Electrolyte disturbances are due to impairment of the intrarenal mechanism of urine dilution due to extracellular fluid volume depletion and inappropriate secretion of antidiuretic hormone. The central nervous system is imminently affected by acute hyponatremia. This condition frequently culminates in cerebral edema, a result of the rapid fluid shift, and causes sudden fatality. Aim of the study This study aims to study dyselectrolytemia in children with severe pneumonia. Objectives The study objectives are to assess dyselectrolytemia in children with severe pneumonia and to correlate dyselectrolytemia with morbidity and hospital stay. Methodology  This prospective study was conducted on 80 children in the age group of two months up to five years who visited our tertiary care center and had severe pneumonia. We evaluated the extent of dyselectrolytemia in our study population by analyzing the frequency correlation of different kinds of electrolyte imbalances. We also analyzed the correlation between morbidity and hospital stay. Results Out of 80 children in this study with severe pneumonia, 47 (59%) had electrolyte imbalance. Among the patients with electrolyte imbalance, 31 (39%) patients had hyponatremia followed by hypokalemia in 12 (15%) patients, hypernatremia in 3 (4%) patients, and hyperkalemia in 1 (1%) patient. Among the 17 (21%) children with pneumonia requiring ICU admission, 16 (94%) had dyselectrolytemia and 4 (24%) experienced fatal outcomes. Conclusions The majority of the children who were admitted to the ICU had severe pneumonia along with electrolyte imbalance. This necessitates the monitoring of the electrolyte and nutritional status of the patients with pneumonia. Providing proper nutrition advice for children with pneumonia may reduce morbidity and mortality. Early detection and treatment of electrolyte imbalances in pneumonia cases can decrease prolonged hospital stays, ICU admissions, and the need for mechanical ventilation, ultimately contributing to a reduction in morbidity and mortality.

Plasma sodium during the recovery of renal function in critically ill adult patients: Multicenter prospective cohort study.

BACKGROUND: Sodium increases during acute kidney injury (AKI) recovery. Both hypernatremia and positive fluid balances are associated with increased mortality. We aimed to evaluate the association between daily fluid balance and daily plasma sodium during the recovery from AKI among critical patients. METHODS: Adult patients with AKI were enrolled in four ICUs and followed up for four days or until ICU discharge or hemodialysis initiation. Day zero was the peak day of creatinine. The primary outcome was daily plasma sodium; the main exposure was daily fluid balance. RESULTS: 93 patients were included. The median age was 66 years; 68% were male. Plasma sodium increased in 79 patients (85%), and 52% presented hypernatremia. We found no effect of daily fluid balance on plasma sodium (ß -0.26, IC95%: -0.63-0.13; p = 0.19). A higher total sodium variation was observed in patients with lower initial plasma sodium (ß -0.40, IC95%: -0.53 to -0.27; p < 0.01), higher initial urea (ß 0.07, IC95%: 0.04-0.01; p < 0.01), and higher net sodium balance (ß 0.002, IC95%: 0.0001-0.01; p = 0.05). CONCLUSIONS: The increase in plasma sodium is common during AKI recovery and can only partially be attributed to the water and electrolyte balances. The incidence of hypernatremia in this population of patients is higher than in the general critically ill patient population.

Severe Burn Injuries - The Day the Sodium Starts Rising.

BACKGROUND/AIM: The current study was designed to evaluate the etiologies of hypernatremic episodes in patients with severe burn injuries in comparison to critically ill non-burn patients. PATIENTS AND METHODS: The retrospective data acquisition was limited to the first 14 days and to patients with at least 20% total body surface area (TBSA) 2nd degree burn injuries or more than 10% TBSA when including areas of 3rd degree burn injuries. The results were compared to the results of a previously published study that analyzed the risk factors for hypernatremia in 390 non-burn intensive care unit patients. RESULTS: In total, 120 patients with a total of 50 hypernatremic episodes were included. Compared to non-burn injury patients, no significant differences were detectable except for a lower rate of hypokalemia and a higher rate of mechanical ventilation. The main trigger for hypernatremic episodes was the loss of free water, while 24% of the hypernatremic episodes seemed to be at least partly triggered by a surplus sodium influx. Patients with hypernatremic episodes had a significantly higher mortality rate. However, in none of the cases was hypernatremia the decisive cause of death. CONCLUSION: Besides the unique phenomenon of high volume internal and external volume shifts, the overall risk factors and etiologies of hypernatremia in patients with severe burn injury do not seem to significantly differ from other ICU patient collectives. Remarkably, a surplus of sodium influx and therefore a modifiable factor besides the specific burn injury volume resuscitation had an impact on the hypernatremic episodes in 24% of cases.

Correction of In-Patient Severe Hypernatremia in an 81-Year-Old Female With Hypopituitarism.

Hypernatremia has been significantly associated with in-hospital mortality and discharge to long-term care facilities. The appropriate correction of electrolyte disturbances, especially sodium, is important to consider to prevent the addition of central nervous system disturbances, such as cerebral edema and eventual brain injury. The importance of maintaining a proper correction of hypernatremia has been well studied and used in clinical practice. Choosing to use a hypotonic solution is a key principle. It is of utmost importance to adjust the rate of correction based on the patient's symptoms, underlying etiology, and associated comorbidities. This case demonstrates how a correction formula was used and adjusted accordingly in an 81-year-old female with severe hypernatremia and metabolic encephalopathy with multiple comorbidities, including hypopituitarism. It is noteworthy to examine the correction rate, how it was calculated and delivered, and how the main cause of the hypernatremia was determined. Considering all these factors can help to properly administer any additional corrective medications, such as desmopressin (DDAVP) in a patient with diabetes insipidus (DI) secondary to hypopituitarism, or adjust the correcting rate based on signs, symptoms, and laboratory findings.