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Intravenous fluids are commonly prescribed to children in hospitals. However, there are risks associated with their use. In order to safely prescribe these clinicians should understand the indications for their use, the principles underpinning their use and know the likely complications associated with intravenous fluid administration in children. Intravenous fluids should be prescribed depending on individual needs of each child and with careful monitoring and re-assessment. This review aims to provide a general approach to fluid prescription in children, providing some background of different physiological principles, different fluid composition, and the role of anti-diuretic hormone in fluid homeostasis. Fluid prescription is discussed, with an approach taking into consideration resuscitation boluses, dehydration, replacing ongoing losses and maintenance requirements. Case examples are provided to further facilitate readers' comprehension. Electrolyte abnormalities and an approach to the management of deranged electrolytes is addressed. Complications associated with fluid administration are highlighted, in particular, emphasizing the assessment and emergency management of the child with suspected cerebral oedema or hyponatraemic encephalopathy. Special consideration and discussion is given to the differing approach to fluid management of children in the setting of burns or diabetic ketoacidosis. [ABSTRACT FROM AUTHOR]

Background The patient described in this case received a diagnosis of severe head trauma that resulted in death. Imaging findings, along with discrepancies in the parental explanation of the incident, aided the forensic investigators to identify the case as nonaccidental trauma (NAT). Discussion Identifying demographic risk factors and performing proper clinical evaluations can serve an important role in the diagnosis of pediatric NAT. Imaging modalities such as radiography, computed tomography, and magnetic resonance imaging can help determine the extent of trauma. Conclusion: Abuse is frequent in the pediatric population. To help prevent future cases of abuse, medical professionals should be fluent in identifying differences between accidental and NAT. Using multiple imaging modalities, NAT in pediatric patients can be identified and treated adequately. [ABSTRACT FROM AUTHOR]

Copyright of Revista Médica Clínica Las Condes is the property of Editorial Sanchez y Barcelo and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

There have been recent advances assessing copeptin levels in adults with suspected disorders of vasopressin release. Very limited data exits on copeptin levels in children and infants, especially in a critically-ill hospitalized population where hyper- and hypo-natremia are very common. Our objective is to describe the institutional experience assessing copeptin levels in hospitalized infants and children with hyper- or hypo-natremia. We performed a single-center retrospective case series of all infants, children, and adolescents who had an ultrasensitive plasma copeptin level obtained between 2019-2021. A total of 29 critically ill patients (6 infants) were identified with 38 % of patients having copeptin levels after neurosurgical procedures for tumors or trauma. Approximately 13/17 children with hypernatremia had central diabetes insipidus (central diabetes insipidus) to diagnose CDI, A copeptin level ≤ 4.9 pmol/L resulted in an 88 % sensitivity (95 % CI 47–99 %), and 66 % specificity (95 % CI 30–93 %). Amongst those with hyponatremia levels were more variable, 8/12 children had syndrome of inappropriate antidiuresis (SIAD) with copeptin levels ranging 4.7–72.6 pmol/L. While difficult to conclude due to multiple limitations, this case series highlights that typical copeptin cutoffs used to diagnose DI in adults in an ambulatory setting may also translate to a critically-ill pediatric population. Large prospective studies are needed to confirm this observation. In addition, postoperative copeptin levels could potentially be utilized as an additional marker to predict permanent from transient DI, but much larger studies are needed. Further work is needed to establish normative copeptin levels in infants and patients with SIAD. [ABSTRACT FROM AUTHOR]

Background: Salt-sensitive hypertension in humans and experimental models is associated with higher plasma and cerebrospinal fluid sodium chloride (NaCl) concentrations. Changes in extracellular NaCl concentrations are sensed by specialized neurons in the organum vasculosum of the lamina terminalis (OVLT). Stimulation of OVLT neurons increases sympathetic nerve activity (SNA) and arterial blood pressure (ABP), whereas chronic activation produces hypertension. Therefore, the present study tested whether OVLT neuronal activity was elevated and contributed to SNA and ABP in salt-sensitive hypertension. Methods: Male Dahl salt-sensitive (Dahl S) and Dahl salt-resistant (Dahl R) rats were fed 0.1% or 4.0% NaCl diets for 3 to 4 weeks and used for single-unit recordings of OVLT neurons or simultaneous recording of multiple sympathetic nerves during pharmacological inhibition of the OVLT. Results: Plasma and cerebrospinal fluid Na+ and Cl− concentrations were higher in Dahl S rats fed 4% versus 0.1% or Dahl R rats fed either diet. In vivo single-unit recordings revealed a significantly higher discharge of NaCl-responsive OVLT neurons in Dahl S rats fed 4% versus 0.1% or Dahl R rats. Interestingly, intracarotid infusion of hypertonic NaCl evoked greater increases in OVLT neuronal discharge of Dahl S versus Dahl R rats regardless of NaCl diet. The activity of non–NaCl-responsive OVLT neurons was not different across strain or diets. Finally, inhibition of OVLT neurons by local injection of the gamma-aminobutyric acid agonist muscimol produced a greater decrease in renal SNA, splanchnic SNA, and ABP of Dahl S rats fed 4% versus 0.1% or Dahl R rats. Conclusions: A high salt diet activates NaCl-responsive OVLT neurons to increase SNA and ABP in salt-sensitive hypertension. [ABSTRACT FROM AUTHOR]

This study was performed to assess the effect of baseline Preoperative Laboratory Values (PLV) on post-operative Brain Tumor Resection (BTR) outcomes in a large national registry. We extracted data from the National Surgical Quality Improvement Program (NSQIP) database for BTR patients 2015–2019 (n = 3 0,951). Uni- and multivariate analyses were performed for PLV and key surgical outcomes. The most significant PLV predictors of 30-day mortality after BTR included hypernatremia (odds ratio, OR 4.184, 95% CI, 2.384–7.343, p < 0.001), high serum creatinine (OR 2.244, 95% CI 1.502–3.352, p < 0.001), thrombocytopenia (OR 1.997, 95% CI 1.438, 2.772, p < 0.001), and leukocytosis (OR 1.635, 95% CI 1.264, 2.116, p < 0.001). The most significant predictors of Clavien IV complications were increased INR (OR 2.653, 95% CI 1.444, 4.875, p < 0.01), thrombocytopenia (OR 1.514, 95% CI 1.280, 1.792, p < 0.001), hypoalbuminemia (OR 1.480, 95% CI 1.274, 1.719, p < 0.001), and leukocytosis (OR 1.467, 95% CI 1.306, 1.647, p < 0.001). The most robust predictors of eLOS were increased INR (OR 1.941, 95% CI 1.231, 3.060, p < 0.01) and hypoalbuminemia (OR 1.993, 95% CI 1.823, 2.179, p < 0.001), and those for non-routine discharge included increased INR (OR 1.897, 95% CI 1.196, 3.008, p < 0.01) and hypernatremia (OR 1.565, 95% CI 1.217, 2.012, p < 0.001). Several PLV independently predicted worse outcomes in BTR patients. Baseline labs should be routinely used for the pre-operative risk stratification of these patients. [ABSTRACT FROM AUTHOR]

Nous présentons ici le cas clinique d'une femme âgée de 54 ans, souffrant d'un trouble bipolaire, suivie en psychiatrie et traitée par lithium, un inhibiteur sélectif de la recapture de sérotonine (escitalopram) et lamotrigine, ayant présenté un tableau d'intoxication au lithium, avec une altération de l'état de conscience, à la suite d'une supposée erreur de gestion de son traitement. L'intoxication au lithium a été suggérée par la présence de symptômes neurologiques et la démonstration biologique d'un taux sérique dans des valeurs thérapeutiques normales à 1,2 mmol/L (N : 0,6–1,2 mmol/L). Les complications biologiques classiques en lien avec une intoxication au lithium (hypercalcémie, diabète insipide) ont conforté le diagnostic. La patiente a été prise en charge dans notre service de néphrologie et a bénéficié d'une épuration extra-rénale qui a conduit à une amélioration clinique et biologique, confortant ainsi le diagnostic d'intoxication au lithium malgré sa lithémie normale. Elle a ensuite été transférée en psychiatrie pour la suite de la prise en charge et l'adaptation du traitement psychotrope. We describe here the case of a 54-year-old bipolar woman, followed in psychiatry and treated with lithium and a selective serotonin reuptake inhibitor (escitalopram) and lamotrigine, presenting a lithium poisoning with an altered state of consciousness caused by a supposed mismanagement of her treatment. Lithium poisoning was suggested based on neurological clinical features, but the blood test brought out a lithium concentration within the therapeutic values at 1,2 mmol/L (N: 0,6–1,2 mmol/L). The classic biological complications related to lithium poisoning (hypercalcemia, diabetes insipidus) confirmed the diagnosis. The patient has been transferred to our nephrology department where she got two hemodialysis sessions conducting to clinical and biological improvement, confirming the diagnosis of lithium poisoning despite the normal blood levels. Later, she was transferred to the psychiatry department for follow-up and for treatment adjustment. [ABSTRACT FROM AUTHOR]

Background: Brain oedema after cardiac arrest is strongly associated with poor neurological outcomes. Excessive sodium supplementation may increase serum osmolarity and facilitate brain oedema development in cardiac arrest survivors. We aimed to investigate the association of serum sodium levels with long-term neurological outcomes in out-of-hospital cardiac arrest (OHCA) survivors.Methods: This retrospective observational study used a multicentre prospective cohort registry of OHCA survivors collected between December 2013 and February 2018. We analyzed the association of serum sodium levels at the return of spontaneous circulation (ROSC) (Sodium 0H) and at 24 h after ROSC (Sodium 24H) with 1-year neurological outcomes in OHCA survivors. Patients with 1-year cerebral performance categories (CPC) 1 and 2 were included in the good outcome group while those with CPC 3, 4, and 5 were included in the poor outcome group.Results: Among 277 patients, 84 (30.3%) and 193 (69.7%) were in the good and poor outcome groups, respectively. Compared with the good outcome group, the poor outcome group showed significantly higher Sodium 24H levels (140 mEq/L vs. 137.4 mEq/L, p < 0.001). Increased serum sodium levels per 1 mEq/L increased the risk of poor 1-year CPC by 13% (adjusted odds ratio = 1.13; 95% CI, 1.04⎼1.23; p = 0.004).Conclusions: Relatively high Sodium 24H levels showed a strong and independent association with poor long-term neurological outcomes in OHCA survivors. These findings may be applied in therapeutic strategies for improving neurological outcomes in OHCA survivors. [ABSTRACT FROM AUTHOR]

Maintenance of electrolyte balance in the neonate is a challenge in the context of illness or prematurity. Neonatal providers' approach to fluid management changes and adapts based on the newborn's age, maintenance needs, deficits, and ongoing losses. Understanding the total body water content of the fetus and newborn is foundational to management of electrolyte disturbances. This article reviews common imbalances of sodium and chloride, identifies causes of imbalances, and discusses current evidence-based treatment options. [ABSTRACT FROM AUTHOR]

Background: Electrolyte levels are commonly obtained as part of the preoperative workup for total joint arthroplasty, but limited information exists on the interplay between electrolyte abnormalities and outcomes.Methods: The National Surgical Quality Improvement Program was queried for primary, elective total hip arthroplasty and total knee arthroplasty (THA, TKA) performed between 2011 and 2017. Three patient groups were compared: normal (control), hypernatremia, and hyponatremia. The primary outcomes were length of stay (LOS) and 30-day adverse events: complications, readmissions, reoperations, and mortality.Results: A total of 244,538 TKAs and 145,134 THAs were analyzed. The prevalence of hyponatremia and hypernatremia was 6.9% and 1.0%, respectively. After controlling for any baseline differences, hypernatremia was an independent predictor of ventilation >48 hours (THA, odds ratio [OR] 3.53), unplanned intubation (THA, OR 3.14), cardiac arrest (THA, OR 2.42), pneumonia (THA, OR 2.16), Clostridium difficile infection (OR 4.66 and 3.25 for THA and TKA, respectively), LOS >2 days (THA, OR 1.16), and mortality (THA, OR 4.69). Similarly, hyponatremia was an independent predictor of LOS >2 days (TKA, OR 1.21), readmission (TKA, OR 1.40), reoperation (OR 1.32 and 1.47 for THA and TKA, respectively), surgical site infections (OR 1.39 and 1.54 for THA and TKA, respectively), and transfusion (OR 1.13 and 1.20 for THA and TKA, respectively).Conclusion: As the focus of total joint arthroplasty continues to shift toward value-based payment models and outpatient surgery, caution should be exercised in patients with abnormal preoperative sodium levels, particularly hypernatremia, because of significantly increased risk of prolonged LOS and 30-day adverse events. [ABSTRACT FROM AUTHOR]

Perioperative sodium abnormalities or dysnatremia is not uncommon in patients presenting for cardiac surgery and is associated with increased morbidity and mortality. Both the disease process of heart failure and its treatment may contribute to abnormalities in serum sodium concentration. Serum sodium is the main determinant of serum osmolality, which in turn affects cell volume. Brain cells are particularly vulnerable to changes in serum osmolality because of the nondistensible cranium. The potentially catastrophic neurologic sequelae of rapidly correcting chronic dysnatremia and the time-sensitive nature of cardiac surgery can make the management of these patients challenging. The use of cardiopulmonary bypass to facilitate surgery adds another layer of complexity in the intraoperative management of sodium and water balance. This narrative review examines the definition and classification of dysnatremia. It also covers the etiology and pathophysiology of dysnatremia, implications during cardiac surgery requiring cardiopulmonary bypass, and the perioperative management of dysnatremia. [ABSTRACT FROM AUTHOR]

Blood glucose and serum sodium abnormalities in very low birth weight infants may cause increased morbidity and mortality, but data regarding the long-term outcomes are limited. This study aimed to investigate the association between the peak and nadir blood glucose and serum sodium levels and neurodevelopmental outcomes in very low birth weight infants. A single-center retrospective medical record of 284 infants with birth weight<1500 g born between February 1, 2011 and January 31, 2015 was reviewed. We analyzed the correlation between peak and nadir blood glucose and serum sodium levels during hospitalization and Bayley Scales of Infant and Toddler Development, third edition at 6, 12, and 24 months of corrected age. A total of 284 very low birth weight premature infants were eligible, and 223, 208, and 188 patients were assessed at 6, 12, and 24 months of corrected age, respectively. Multiple linear regression analysis with generalized estimating equations showed that the BSID-III cognitive scores were significantly lower in the peak serum sodium group when sodium was ≧150 mmol/L (95% confidence interval −11.681 to −0.822) than when sodium did not exceed 150 mmol/L. A peak serum sodium of ≧150 mmol/L is associated with poor cognitive outcomes in very low birth weight infants. Further studies are necessary to determine if this association is causal or an expression of disease severity. [ABSTRACT FROM AUTHOR]

To evaluate associations between clinicopathological variables and hypercapnia measured in cats with decompensated chronic kidney disease (CKD) on admission to a veterinary hospital. This is a retrospective, cross-sectional study of cats (n = 39) that presented to a tertiary veterinary hospital in Argentina between June 2015 and December 2017 with blood creatinine concentrations >140 μmol/L, and abdominal ultrasound results consistent with CKD. Data recorded included venous partial pressure of CO2 (PvCO2), blood pH, haematocrit and concentrations of glucose, potassium, sodium, corrected sodium (Na+c), and ionised calcium in blood. A logistic regression model was used to assess associations between the presence of hypercapnia (PvCO2 ≥ 44.7 mmHg) and the other clinicopathologic variables. The duration of hospitalisation was compared in cats with and without hypercapnia using the Wilcoxon Rank Sum test. The final study population comprised 39 cats. Eleven cats (28.2%) had hypercapnia. In the logistic regression model, two independent variables were associated with the presence of hypercapnia at admission in cats with CKD: the concentration of creatinine in blood (OR = 1.06 (95% CI = 1.016–1.108); p = 0.007) and Na+c (OR = 1.33 (95% CI = 1.08–1.63); p = 0.005). There were no statistically significant differences in the length of hospital stay between the two groups. There appears to be an association between elevated concentrations of creatinine and Na+c in blood, and hypercapnia in cats with CKD, suggesting careful assessment of blood gas and electrolyte parameters during hospitalisation is required. Further prospective studies are needed to evaluate the mechanisms behind this association and the association of hypercapnia with disease outcome including mortality. [ABSTRACT FROM AUTHOR]

[Figure: see text]. [ABSTRACT FROM AUTHOR]

• DNC/BD requires exclusion of severe electrolytes, acid/base or endocriniologic derangements. • Many DNC/BD guidelines do not define metabolic testing or values that preclude diagnosis. • Neurointensivists commonly check sodium, arterial pH, and glucose prior to evaluation of DNC/BD. • Independent of experience, neurointensivists use similar laboratory values for exclusion. There are no established ranges for metabolic values prior to death by neurologic criteria/brain death determination (DNC/BD) and the thresholds required by institutional protocols and accepted by neurointensivists is unknown. We designed a survey that addressed 1) the metabolic tests required in institutional guidelines prior to brain death determination, 2) the metabolic tests the respondent reviewed prior to brain death determination, and 3) the metabolic test thresholds for laboratory tests that were perceived to preclude or permit clinical DNC/BD determination. The survey was distributed online to physicians in the Neurocritical Care Society from September to December 2019. Respondents were dichotomized based on the number of brain death evaluations they had performed (≤20 vs. > 20) and responses were compared between groups. The survey was completed by 84 physicians. Nearly half (47.6%) of respondents did not believe their institutions required metabolic testing. The metabolic testing for which institutions most commonly provided a defined threshold were arterial pH (34.5%, 29/84), sodium (28.6%, 24/84), and glucose (15.5%, 13/84). Nearly all (97.6%) respondents routinely reviewed metabolic tests prior to brain death evaluation, the most common of which were: sodium (91.7%, 77/84), arterial pH (83.3%, 70/84), and glucose (79.8%, 67/84). Respondents who had performed > 20 evaluations were less likely to check thyroxine and total bilirubin (3.6%, 2/55 vs. 20.7%, 6/29 (p = 0.011) and 12.7%, 7/55 vs. 31%, 9/29 (p = 0.042), respectively), and had a more liberal upper limit of potassium (6.3 mEq/L vs 6.0 mEq/L, p = 0.045). Prior to brain death evaluation, neurocritical care providers commonly review similar metabolic tests and have similar thresholds regarding values that would preclude clinical brain death determination. This finding is independent of experience with brain death determination. [ABSTRACT FROM AUTHOR]

Background: Standardized parenteral nutrition (PN) formulations are used in at-risk neonates to provide nutrition immediately following birth. However, evidence for the optimal formulation(s) to maximize growth while reducing the risks of glucose and electrolyte abnormalities is limited.Purpose: The purpose of this study was to compare the rates of hypernatremia and hyperglycemia with 2 weight-based standardized PN formulations versus one standard PN in low birth-weight preterm neonates.Methods: This was a single-center observational study of infants less than 1800 g birth weight and less than 37 weeks' gestation who received standardized PN in the first 48 hours of life. Patients in the weight-based PN group were compared with a historical group of patients receiving single standard PN. Rates of hypernatremia and hyperglycemia were compared by χ2 analysis.Results: There was a nonsignificant (P = .147) reduction in hypernatremia in the weight-based PN group (9 of 87; 10.3%) compared with the single PN group (16 of 89; 18.0%). However, hyperglycemia was significantly more frequent in the weight-based group than in the single PN group (24.1% vs 12.4%, P = .035).Implications For Practice: The 2 weight-based PN standardized formulations studied did not significantly decrease the incidence of hypernatremia or hyperglycemia.Implications For Research: Future studies to determine optimal standardized PN to provide early nutrition in high-risk neonates are warranted. [ABSTRACT FROM AUTHOR]

Purpose: We aimed to investigate the prevalence, risk factors and outcome of hypo- and hypernatremia in emergency patients with acute kidney injury (AKI).Methods: In this cross-sectional analysis all emergency patients between January 1st 2017 and December 31st 2018 with measurements of creatinine and sodium were included. Baseline characteristics, medication and laboratory data were gathered. Chart reviews were performed to identify patients with a diagnosis of chronic kidney disease (CKD) and to extract baseline creatinine. For all other patients the ADQI backformula was used to calculate baseline creatinine. AKI was graduated using creatinine criteria of the acute kidney injury network. Binary logistic regression analysis was used to identify risk factors for appearance of dysnatremias and outcome.Results: AKI was found in 8% of patients. 392 patients (23.16%) had hyponatremia, 24 (1.4%) had hypernatremia. Use of potassium sparing diuretics, a medical cause for emergency referral, use of thiazide diuretics and AKI stage were the strongest risk factors for hyponatremia. Loop diuretics, a medical cause for emergency referral and AKI stage were risk factors for hypernatremia. In patients with all classes of hyponatremia, length of hospital stay was significantly longer compared to patients with a normal serum sodium. In the binary logistic regression analysis with death as outcome, hyponatremia as well as severe hypernatremia were independent risk factors for mortality.Conclusions: Dysnatremias are common in emergency patients with AKI. Diuretic medication is a major risk factor for hypo- and hypernatremia. Both hyponatremia and severe hypernatremia were independent risk factors for adverse outcome. [ABSTRACT FROM AUTHOR]

Central or neurogenic diabetes insipidus (DI) is uncommon in the pediatric age group and rarely occurs in neonates. It should be suspected in any neonate presenting with excessive urine output and hypernatremia that persists despite increased fluid administration. Diabetes insipidus may be secondary to asphyxia, intraventricular hemorrhage, infection, and structural abnormalities or may be idiopathic or genetic. Diagnosis includes a careful history, laboratory testing, and magnetic resonance imaging. Management of neonatal DI involves a careful balance between fluid intake and pharmacologic treatment. In this article we report a case of an extremely low birth weight infant presenting with central DI possibly caused by abnormality of the pituitary gland. Persistent hypernatremia was the initial presentation. Increased fluids were given initially but were only partially helpful. Eventually subcutaneous desmopressin (DDAVP) was required. The infant was unresponsive to intranasal DDAVP and required subcutaneous DDAVP upon discharge. [ABSTRACT FROM AUTHOR]

Safe intravenous fluid prescription in children requires an understanding of certain basic principles to avoid adverse events. Careful consideration needs to be given to both the appropriate rate and composition of the fluids to be administered with frequent re-assessment. This review will examine the indications for parenteral fluid management; maintenance requirements, correction of any deficit and replacement of ongoing losses. The role of non-osmotic secretion of anti-diuretic hormone (ADH) is discussed and children at particular risk are identified. We review complications associated with intravenous fluid therapy, in particular hyponatraemic encephalopathy and discuss the management of this medical emergency. Other electrolyte abnormalities that may arise are highlighted. Fluid management in children with diabetic ketoacidosis is also reviewed. [ABSTRACT FROM AUTHOR]

Objective: The objectives of this study were to evaluate the current practice of postoperative fluid prescribing and assess the effectiveness of pharmacist-led intervention in the implementation of the National Institute of Health and Care Excellence (NICE) fluid therapy guideline in an Iraqi hospital. Methods: The prospective interventional study was conducted at AL-Hilla Teaching Hospital, Babylon, Iraq between November 2017 and July 2018. The study included two phases: The pre-intervention phase with 84 patients and the post-intervention phase with 112 patients. A pharmacist provided training and educational sessions for the hospital physicians and pharmacists about the NICE guideline of fluid therapy. The researcher calculated the amount of given post-operative fluids and compared to the NICE guideline and also measured the patients' body weight, serum Na, K and creatinine pre-and post-operatively. Results: The pre-intervention phase showed no correlation between the amounts of prescribed fluids and body weight which caused increases in patients' body weight. In pre-intervention phase, 6% of patients experienced hyponatremia, 19% had hypernatremia and 7.1% had hypokalemia. In the post-intervention phase, abnormal level of electrolytes and patient weight gain decreased significantly. Additionally, the intervention led to a strong correlation between body weight and amount of prescribed fluids in addition to lowering the incidence of electrolyte disturbances. Conclusions: A high proportion of patients in the pre-intervention phase experienced fluid overload, weight gain and electrolyte disturbances when fluid therapy was not prescribed in accordance with the NICE guidelines. The pharmacist-led intervention increased the surgeon awareness of the proper use of the NICE guideline which decreased the incidence of fluid-related complications and the inconsistency of fluid prescribing. Pharmacists can play a critical role to enhance post-operative fluid prescribing and minimize fluid-induced complications. [ABSTRACT FROM AUTHOR]

Background: Idiopathic central diabetes insipidus (CDI) has been associated with intracranial pathologies that do not involve the structural pituitary gland or hypothalamus. The objective was to study the association between non-structural hypothalamic/pituitary intracranial pathologies (NSHPIP) with CDI and to review etiologies that may be contributory to the development of CDI. Methods: A retrospective query of our intra-institutional database from 2006 to 2015. Children admitted diagnosed with diabetes insipidus (DI) (ICD-9 253.5) between the ages of 0–1 year were included. Patient charts were reviewed to include those who have a documented diagnosis of CDI, hypernatremia (>145 mmol/L), high serum osmolality (>300 mOsm/kg), low urine osmolality (<300 mOsm/kg), and brain imaging reports. Diagnoses of nephrogenic DI were excluded. Results: Twenty-three infant patients were diagnosed with CDI. Eleven subjects (48%) had NSHPIP. Of those, 18% had cerebral infarction, 27% had intracranial injury and hemorrhage due to traumatic brain injury, 18% had isolated intraventricular hemorrhage, and 27% had meningitis. Hospital prevalence for NSHPIP, age 0–1 year, ranged from 0.05% to 0.3%. Conclusions: Rates of NSHPIP in those with CDI are higher than expected hospital rates (p<0.001), suggesting a possible association between CDI and NSHPIP. [ABSTRACT FROM AUTHOR]

Copyright of Scientia Medica is the property of EDIPUCRS - Editora Universitaria da PUCRS and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: Dysnatremia and altered hydration status are potentially serious conditions that have not been well studied in multistage ultramarathons. The purpose of this study was to assess the incidence and prevalence of exercise-associated hyponatremia (EAH) (Na+ <135 mmol·L-1) and hypernatremia (Na+ >145 mmol·L-1) and hydration status during a multistage ultramarathon.Methods: This study involved a prospective observational cohort study of runners competing in a 250-km (155-mile) multistage ultramarathon (in the Jordan, Atacama, or Gobi Desert). Prerace body weight and poststage (stage [S] 1 [42 km], S3 [126 km], and S5 [250 km]) body weight and serum sodium concentration levels were obtained from 128 runners.Results: The prevalence of EAH per stage was 1.6% (S1), 4.8% (S3), and 10.1% (S5) with a cumulative incidence of 14.8%. Per-stage prevalence of hypernatremia was 35.2% (S1), 20.2% (S3), and 19.3% (S5) with a cumulative incidence of 52.3%. Runners became more dehydrated (weight change <-3%) throughout the race (S1=22.1%; S3=51.2%; S5=53.5%). Body weight gain correlated with EAH (r=-0.21, P = .02). Nonfinishers of S3 were significantly more likely to have EAH compared with finishers (75% vs 5%, P = .001), but there was no difference in either EAH or hypernatremia between nonfinishers and finishers of S5.Conclusions: The incidence of EAH in multistage ultramarathons was similar to marathons and single-stage ultramarathons, but the cumulative incidence of hypernatremia was 3 times greater than that of EAH. EAH was associated with increased weight gain (overhydration) in early stage nonfinishers and postrace finishers. [ABSTRACT FROM AUTHOR]

According to the American Academy of Pediatrics (2012), breastfeeding is the optimal way to provide nutrition to newborns. Over the last several years, breastfeeding has increased in popularity. There are many documented positive effects of breastfeeding to the infant. Neonatal hypernatremia is a potential complication resulting from inadequate milk transfer and dehydration that can occur in infants who are exclusively breastfed. Although rare, neonatal hypernatremia can be easily prevented with appropriate parental education. [ABSTRACT FROM AUTHOR]

A 40-year-old man was admitted to the hospital with multiple injuries, including head injury and his laboratory results were significant for sodium abnormalities. Initially, hypernatremia was from increased sodium intake. Subsequently, hyponatremia developed that was unresponsive to sodium supplementation. Syndrome of inappropriate antidiuretic hormone secretion or cerebral salt wasting syndrome was suspected. Additional tests suggested post-traumatic hypopituitarism was responsible for the hyponatremia. Corticosteroid were given which normalized the serum sodium level, but the urine volume increased. Masked diabetes insipidus was suspected and desmopressin was given, stabilizing the serum sodium level. Recognizing the factors that cause sodium abnormalities in trauma patients can help lead to the correct diagnosis. [ABSTRACT FROM AUTHOR]

• Nephrogenic diabetes insipidus can occur years after lithium discontinuation. • Life-threatening hypernatremia can develop post-operatively. • Inappropriate fluid resuscitation worsens post-operative hypernatremia. • High clinical suspicion and close monitoring are essential in the post-operative period. Nephrogenic diabetes insipidus occurs in patients on chronic lithium treatment even after lithium discontinuation. Patients affected by this disorder are highly vulnerable to hypernatremia when they cannot respond to their thirst mechanism. We report a rare case of hypernatremia due to undiagnosed nephrogenic diabetes insipidus post esophagectomy in a patient with remote history of lithium use. A 70-year-old female with past medical history of bipolar disorder, chronic kidney disease and pheochromocytoma underwent an elective esophagectomy for esophageal adenocarcinoma. Lithium was discontinued 10 years prior to her presentation. She was kept nil per os post operatively and subsequently developed altered mental status necessitating intubation. Her sodium level was found to be 156 mmol/L. A water deprivation test and desmopressin trial confirmed nephrogenic diabetes insipidus. Days after dextrose 5% in water infusion, free water flushes through the jejunostomy tube and hydrochlorothiazide, her hypernatremia improved slowly with subsequent improvement in her mental status. Several mechanisms have been described in literature to explain the persistent damage caused by lithium on the kidneys. When patients lose access to a source of free water and are resuscitated with normal saline post operatively, they are at risk of developing life-threatening hypernatremia. This can be avoided by aggressive hydration with appropriate fluid replacement. Surgeons should be aware of the persistent renal defects caused by long term lithium use and development of nephrogenic diabetes insipidus even years after medication cessation. [ABSTRACT FROM AUTHOR]

Copyright of Revista Medica Herediana is the property of Universidad Peruana Cayetano Heredia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Primary hypodipsic hypernatremia is a rarely reported disease in dogs. Reported underlying causes associated with this disease in dogs include congenital malformations, encephalitis, intracranial neoplasia, and pressure atrophy of the hypothalamus secondary to hydrocephalus. The dog in this report had an infiltrative neoplastic disorder, likely causing damage to the hypothalamic osmoreceptors responsible for the thirst generation. The neoplastic process was identified histopathologically as glioblastomamultiforme, an unusual tumor to occur in a dog this young. A tumor of the central nervous system causing physical destruction of the osmoreceptors has rarely been reported in dogs and none of the previously reported cases involved a glial cell tumor. [ABSTRACT FROM AUTHOR]

Hypernatremia (serum sodium concentration >145 mEq/L) is a common electrolyte disorder with increased morbidity and mortality especially in the elderly and critically ill patients. The review presents the main pathogenetic mechanisms of hypernatremia, provides specific directions for the evaluation of patients with increased sodium levels and describes a detailed algorithm for the proper correction of hypernatremia. Furthermore, two representative cases of hypovolemic and hypervolemic hypernatremia are presented along with practical clues for their proper evaluation and treatment. Accurate diagnosis and appropriate treatment is crucial since undercorrection or overcorrection of hypernatremia are both associated with poor patients’ prognosis. [ABSTRACT FROM PUBLISHER]

Hypernatremia is defined as a serum sodium level above 145 mmol/L. It is a frequently encountered electrolyte disturbance in the hospital setting, with an unappreciated high mortality. Understanding hypernatremia requires a comprehension of body fluid compartments, as well as concepts of the preservation of normal body water balance. The human body maintains a normal osmolality between 280 and 295 mOsm/kg via Arginine Vasopressin (AVP), thirst, and the renal response to AVP; dysfunction of all three of these factors can cause hypernatremia. We review new developments in the pathophysiology of hypernatremia, in addition to the differential diagnosis and management of this important electrolyte disorder. [ABSTRACT FROM AUTHOR]