Protein-based oral rehydration solutions for patients with an ileostomy: A randomised, double-blinded crossover study.

BACKGROUND & AIM: Patients with an ileostomy are at increased risk of dehydration and sodium depletion. Treatments recommended may include oral rehydration solutions (ORS). We aimed to investigate if protein type or protein hydrolysation affects absorption from iso-osmolar ORS in patients with an ileostomy. METHODS: This was a randomised, double-blinded, active comparator-controlled 3 × 3 crossover intervention study. We developed three protein-based ORS with whey protein isolate, caseinate or whey protein hydrolysate. The solutions contained 40-48 g protein/L, 34-45 mmol sodium/L and had an osmolality of 248-270 mOsm/kg. The patients ingested 500 mL/d. The study consisted of three 4-week periods with a >2-week washout between each intervention. The primary outcome was wet-weight ileostomy output. Ileostomy output and urine were collected for a 24-h period before and after each intervention. Additionally, blood sampling, dietary records, muscle-strength tests, bioimpedance analyses, questionnaires and psychometric tests were conducted. RESULTS: We included 14 patients, of whom 13 completed at least one intervention. Ten patients completed all three interventions. Wet-weight ileostomy output did not change following either of the three interventions and did not differ between interventions (p = 0.38). A cluster of statistically significant improvements related to absorption was observed following the intake of whey protein isolate ORS, including decreased faecal losses of energy (-365 kJ/d, 95% confidence interval (CI), -643 to -87, p = 0.012), potassium (-7.8 mmol/L, 95%CI, -12.0 to -3.6, p = 0.001), magnesium (-4.0 mmol/L, 95%CI, -7.4 to -0.7, p = 0.020), improved plasma aldosterone (-4674 pmol/L 95%CI, -8536 to -812, p = 0.019), estimated glomerular filtration rate (eGFR) (2.8 mL/min/1.73 m2, 95%CI, 0.3 to 5.4, p = 0.03) and CO2 (1.7 mmol/L 95%CI, 0.1 to 3.3, p = 0.04). CONCLUSION: Ingestion of 500 mL/d of iso-osmolar solutions containing either whey protein isolate, caseinate or whey protein hydrolysate for four weeks resulted in unchanged and comparable ileostomy outputs in patients with an ileostomy. Following whey protein isolate ORS, we observed discrete improvements in a series of absorption proxies in both faeces and blood, indicating increased absorption. The protein-based ORS were safe and well-tolerated. Treatments should be tailored to each patient, and future studies are warranted to explore treatment-effect heterogeneity and whether different compositions or doses of ORS can improve absorption and nutritional status in patients with an ileostomy. GOV STUDY IDENTIFIER: NCT04141826.

How a positive fluid balance develops in acute kidney injury: A binational, observational study.

PURPOSE: A positive fluid balance (FB) is associated with harm in intensive care unit (ICU) patients with acute kidney injury (AKI). We aimed to understand how a positive balance develops in such patients. METHODS: Multinational, retrospective cohort study of critically ill patients with AKI not requiring renal replacement therapy. RESULTS: AKI occurred at a median of two days after admission in 7894 (17.3%) patients. Cumulative FB became progressively positive, peaking on day three despite only 848 (10.7%) patients receiving fluid resuscitation in the ICU. In those three days, persistent crystalloid use (median:60.0 mL/h; IQR 28.9-89.2), nutritional intake (median:18.2 mL/h; IQR 0.0-45.9) and limited urine output (UO) (median:70.8 mL/h; IQR 49.0-96.7) contributed to a positive FB. Although UO increased each day, it failed to match input, with only 797 (10.1%) patients receiving diuretics in ICU. After adjustment, a positive FB four days after AKI diagnosis was associated with an increased risk of hospital mortality (OR 1.12;95% confidence intervals 1.05-1.19;p-value <0.001). CONCLUSION: Among ICU patients with AKI, cumulative FB increased after diagnosis and was associated with an increased risk of mortality. Continued crystalloid administration, increased nutritional intake, limited UO, and minimal use of diuretics all contributed to positive FB. KEY POINTS: Question How does a positive fluid balance develop in critically ill patients with acute kidney injury? Findings Cumulative FB increased after AKI diagnosis and was secondary to persistent crystalloid fluid administration, increasing nutritional fluid intake, and insufficient urine output. Despite the absence of resuscitation fluid and an increasing cumulative FB, there was persistently low diuretics use, ongoing crystalloid use, and a progressive escalation of nutritional fluid therapy. Meaning Current management results in fluid accumulation after diagnosis of AKI, as a result of ongoing crystalloid administration, increasing nutritional fluid, limited urine output and minimal diuretic use.

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.

Classifying Hypotonic Hyponatremia by Projected Treatment Effects - A Quantitative 3-Dimensional Framework.

Introduction: The diagnostic algorithms currently used for hypotonic hyponatremia focus primarily on impaired urinary dilution and often neglect the influence of free water intake and solute excretion. We hypothesized that, in each case of hypotonic hyponatremia different pathophysiological mechanisms play a role simultaneously. Methods: Using clinical data of the previous observational Co-Med study, we defined each case of hypotonic hyponatremia concurrently in 3 dimensions as follows: (i) high net free water intake (HNFWI), (ii) impaired dilution of the urine (IDU), and (iii) low nonelectrolyte solute excretion (LNESE). For each dimension, a "standard delta sodium" (sdna) was calculated reflecting the expected difference to the serum sodium concentration, that would result from changing a dimension to a specific and equivalent target level. Results: Results from 279 patients were used for this analysis. With target levels of free water intake and urine osmolality at the fifth percentile, and nonelectrolyte solute excretion at the 95th percentile, median (interquartile range) sdna values were 7.1 (4.8-10.2) for HNFWI, 11.8 (7.0-18.6) for IDU and 2.6 (1.6-4.2) mmol/l per 24 hours for LNESE. Sdna results in individual patients were highest with IDU in 68.5%, HNFWI in 30.8% and 0.7% with LNESE. At an sdna-level of at least 4mmol/l per 24 hours, the prevalence of HNFWI was 78.9%, IDU 87.1%, and LNESE 26.5%. 77.5% of patients had 2 or all 3 mechanisms present. Hyponatremia was mostly multifactorial in subgroups according to classic categories of hyponatremia and typical comorbidities as well. Conclusion: Hypotonic hyponatremia can be quantitatively defined by 3 dimensions. Most cases should be considered multifactorial.

New horizons in the diagnosis and management of dehydration.

Hydration is a fundamental aspect of clinical practice and yet it is an under-researched topic, particularly in older people, leading to many areas of uncertainty. There are two types of dehydration; hypertonic, which is a water deficit, and isotonic, which is a deficit of both water and salt. Individual clinical signs and bedside tests are poor diagnostic tools, making dehydration difficult to identify. However, the diagnostic value of a holistic clinical approach is not known. The gold-standard clinical test for dehydration is serum osmolality, but this cannot diagnose isotonic dehydration and may delay diagnosis in acute situations. Salivary osmolality point-of-care testing is a promising and rapid new diagnostic test capable of detecting both hypertonic and isotonic dehydration in older people, but further evidence to support its clinical utility is needed. Daily fluid requirements may be less than previously thought in adults, but the evidence specific to older people remains limited. Hydration via the subcutaneous route is safer and easier to initiate than the intravenous route but is limited by infusion speed and volume. Prompting older adults more frequently to drink, offering a wider selection of drinks and using drinking vessels with particular features can result in small increases in oral intake in the short-term. The ongoing clinically-assisted hydration at end of life (CHELsea II) trial will hopefully provide more evidence for the emotive issue of hydration at the end of life.

[Hyponatremia : Etiology, diagnosis and acute therapy]. / Hyponatriämie : Ätiologie, Diagnostik und Akuttherapie.

Hyponatremia is one of the most common electrolyte disorders in emergency departments and hospitalized patients. Serum sodium concentration is controlled by osmoregulation and volume regulation. Both pathways are regulated via the release of antidiuretic hormone (ADH). Syndrome of inappropriate release of ADH (SIADH) may be caused by neoplasms or pneumonia but may also be triggered by drug use or drug abuse. Excessive fluid intake may also result in a decrease in serum sodium concentration. Rapid alteration in serum sodium concentration leads to cell swelling or cell shrinkage, which primarily causes neurological symptoms. The dynamics of development of hyponatremia and its duration are crucial. In addition to blood testing, a clinical examination and urine analysis are essential in the differential diagnosis of hyponatremia.

Evidence-based hyponatremia management in liver disease.

Hyponatremia is primarily a water balance disorder associated with high morbidity and mortality. The pathophysiological mechanisms behind hyponatremia are multifactorial, and diagnosing and treating this disorder remains challenging. In this review, the classification, pathogenesis, and step-by-step management approaches for hyponatremia in patients with liver disease are described based on recent evidence. We summarize the five sequential steps of the traditional diagnostic approach: 1) confirm true hypotonic hyponatremia, 2) assess the severity of hyponatremia symptoms, 3) measure urine osmolality, 4) classify hyponatremia based on the urine sodium concentration and extracellular fluid status, and 5) rule out any coexisting endocrine disorder and renal failure. Distinct treatment strategies for hyponatremia in liver disease should be applied according to the symptoms, duration, and etiology of disease. Symptomatic hyponatremia requires immediate correction with 3% saline. Asymptomatic chronic hyponatremia in liver disease is prevalent and treatment plans should be individualized based on diagnosis. Treatment options for correcting hyponatremia in advanced liver disease may include water restriction; hypokalemia correction; and administration of vasopressin antagonists, albumin, and 3% saline. Safety concerns for patients with liver disease include a higher risk of osmotic demyelination syndrome.

Sodium depletion and secondary hyperaldosteronism in outpatients with an ileostomy: a cross-sectional study.

OBJECTIVE: Patients with an ileostomy may experience postoperative electrolyte derangement and dehydration but are presumed to stabilise thereafter. We aimed to investigate the prevalence of sodium depletion in stable outpatients with an ileostomy and applied established methods to estimate their fluid status. METHODS: We invited 178 patients with an ileostomy through a region-wide Quality-of-Life-survey to undergo outpatient evaluation of their sodium and fluid status. The patients delivered urine and blood samples, had bioelectrical impedance analysis performed and answered a questionnaire regarding dietary habits. RESULTS: Out of 178 invitees, 49 patients with an ileostomy were included; 22 patients (45%, 95% CI, 31-59%) had unmeasurably low urinary sodium excretion (<20 mmol/L), indicative of chronic sodium depletion, and 26% (95% CI, 16-41%) had plasma aldosterone levels above the reference value. Patients with unmeasurably low urinary sodium excretion had low estimated glomerular filtration rates (median 76, IQR 63-89, mL/min/1.73m2) and low venous blood plasma CO2 (median 24, IQR 21-26, mmol/L), indicative of chronic renal impairment and metabolic acidosis. Bioelectrical impedance analysis, plasma osmolality, creatinine and sodium values were not informative in determining sodium status in this population. CONCLUSION: A high proportion of patients with an ileostomy may be chronically sodium depleted, indicated by absent urinary sodium excretion, secondary hyperaldosteronism and chronic renal impairment, despite normal standard biochemical tests. Sodium depletion may adversely affect longstanding renal function. Future studies should investigate methods to estimate and monitor fluid status and aim to develop treatments to improve sodium depletion and dehydration in patients with an ileostomy.IMPACT AND PRACTICE RELEVANCE STATEMENTSodium depletion in otherwise healthy persons with an ileostomy was identified in a few publications from the 1980s. The magnitude of the problem has not been demonstrated before. The present study quantifies the degree of sodium depletion and secondary hyperaldosteronism in this group, and the results may help guide clinicians to optimise treatment. Sodium depletion is easily assessed with a urine sample, and sequelae may possibly be avoided if sodium depletion is detected early and treated. This could ultimately help increase the quality of life in patients with an ileostomy.

Poliuria post-obstructiva. Análisis fisiopatológico de un caso / Post-obstructive polyuria. Pathophysiological analysis of a case

The relief of the impediment to urinary flow is the treatment of acute kidney failure due to urinary tract obstruction. However, there is a risk of inducing massive polyuria, which can be self-limited or produce severe contraction of the intravascular volume with pre-renal acute kidney failure and alterations in the internal environment. Polyuria, urine output > 3 L/d or > 200 mL/min for more than 2 hours, can have multiple causes, and can be classified as osmotic, aqueous or mixed. Post-obstructive polyuria obeys different pathogenic mechanisms, which overlap and vary during a patient's evolution. Initially, there is a decrease in vasoconstrictor factors and an increase in renal blood flow, which, added to the excess of urea accumulated, will cause intense osmotic diuresis (osmotic polyuria due to urea). Added to these factors are the positive sodium and water balance during acute renal failure, plus the contributions of crystalloid solutions to replace diuresis (ionic osmotic polyuria). Finally, there may be tubular dysfunction and decreased solutes in the renal medullary interstitium, adding resistance to the action of vasopressin. The latter causes a loss of free water (mixed polyuria). We present the case of a patient with post-obstructive polyuria where, by analyzing the clinical symptoms and laboratory alterations, it was possible to interpret the mechanisms of polyuria and administer appropriate treatment for the pathogenic mechanism.

Tumor Lysis Syndrome Rare Presentation As Uremic Pericarditis: A Case Report.

Tumor lysis syndrome (TLS) is an oncological emergency characterized by the massive destruction of malignant cells and the release of their contents into the extracellular space, which might occur spontaneously or post-chemotherapy. According to the Cairo&Bishop Classification, it can be defined by both laboratory criteria: hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia (two or more); and clinical criteria: acute kidney injury (AKI), convulsions, arrhythmias, or death. We report the case of a 63-year-old man with a previous medical history of colorectal carcinoma and associated multiorgan metastasis. The patient was initially admitted to the Coronary Intensive Care Unit, five days after the chemotherapy session, on suspicion of Acute Myocardial Infarction. Upon admission, he presented without significant elevation of myocardial injury markers, but with laboratory abnormalities (hyperkalemia, hyperphosphatemia, hyperuricemia, and hypocalcemia) and clinical symptoms (sudden sharp chest pain with pleuritic characteristics and electrocardiographic anomalies suggesting uremic pericarditis, and acute kidney injury), all consistent with TLS. The best approach to established TLS is aggressive fluid therapy and a decrease in uric acid levels. Rasburicase proved to be notoriously more effective, both in terms of prevention and treatment of established TLS, thus consisting of the first-line drug. However, in the present case, rasburicase was not available at the hospital level, so a decision was made to initiate treatment with allopurinol. The case evolved with slow but good clinical evolution. Its uniqueness resides in its initial presentation as uremic pericarditis, scarcely described in the literature. The constellation of metabolic alterations from this syndrome translates into a spectrum of clinical manifestations that can go unnoticed and ultimately may prove to be fatal. Its recognition and prevention are crucial for improving patient outcomes.

The Clinical Characteristics of Electrolyte Disturbance in Patients with Moderate and Severe Traumatic Brain Injury Who Underwent Craniotomy and Its Influence on Prognosis.

OBJECTIVE: The present study aimed to investigate the clinical characteristics of electrolyte imbalance in patients with moderate to severe traumatic brain injury (TBI) who underwent craniotomy and its influence on prognosis. METHODS: A total of 156 patients with moderate to severe TBI were prospectively collected from June 2019 to June 2021. All patients underwent craniotomy and intracranial pressure (ICP) monitoring. We aimed to explore the clinical characteristics of electrolyte disturbance and to analyze the influence of electrolyte disturbance on prognosis. RESULTS: A total of 156 patients with moderate and severe TBI were included. There were 57 cases of hypernatremia, accounting for 36.538%, with the average level of 155.788±7.686 mmol/L, which occurred 2.2±0.3 days after injury. There were 25 cases of hyponatremia, accounting for 16.026%, with the average level of 131.204±3.708 mmol/L, which occurred 10.2±3.3 days after injury. There were three cases of hyperkalemia, accounting for 1.923%, with the average level of 7.140±1.297 mmol/L, which occurred 5.3±0.2 days after injury. There were 75 cases of hypokalemia, accounting for 48.077%, with the average level of 3.071±0.302 mmol/L, which occurred 1.8±0.6 days after injury. There were 105 cases of hypocalcemia, accounting for 67.308%, with the average level of 1.846±0.104 mmol/L, which occurred 1.6±0.2 days after injury. There were 17 cases of hypermagnesemia, accounting for 10.897%, with the average level of 1.213±0.426 mmol/L, which occurred 1.8±0.5 days after injury. There were 99 cases of hypomagnesemia, accounting for 63.462%, with the average level of 0.652±0.061 mmol/L, which occurred 1.3±0.4 days after injury. Univariate regression analysis revealed that age, Glasgow coma scale (GCS) score at admission, pupil changes, ICP, hypernatremia, hypocalcemia, hypernatremia combined with hypocalcemia, epilepsy, cerebral infarction, severe hypoproteinemia were statistically abnormal (p<0.05), while gender, hyponatremia, potassium, magnesium, intracranial infection, pneumonia, allogeneic blood transfusion, hypertension, diabetes, abnormal liver function, and abnormal renal function were not statistically significant (p>0.05). After adjusting gender, age, GCS, pupil changes, ICP, epilepsy, cerebral infarction, severe hypoproteinemia, multivariate logistic regression analysis revealed that hypernatremia or hypocalcemia was not statistically significant, while hypernatremia combined with hypocalcemia was statistically significant (p<0.05). CONCLUSION: The incidence of hypocalcemia was the highest, followed by hypomagnesemia, hypokalemia, hypernatremia, hyponatremia and hypermagnesemia. Hypocalcemia, hypomagnesemia, and hypokalemia generally occurred in the early post-TBI period, hypernatremia occurred in the peak period of ICP, and hyponatremia mostly occurred in the late period after decreased ICP. Hypernatremia combined with hypocalcemia was associated with prognosis.

Cerebrospinal fluid and arterial acid-base equilibria in spontaneously breathing third-trimester pregnant women.

BACKGROUND: Acid-base status in full-term pregnant women is characterised by hypocapnic alkalosis. Whether this respiratory alkalosis is primary or consequent to changes in CSF electrolytes is not clear. METHODS: We enrolled third-trimester pregnant women (pregnant group) and healthy, non-pregnant women of childbearing age (controls) undergoing spinal anaesthesia for Caesarean delivery and elective surgery, respectively. Electrolytes, strong ion difference (SID), partial pressure of carbon dioxide ( [Formula: see text] ), and pH were measured in simultaneously collected CSF and arterial blood samples. RESULTS: All pregnant women (20) were hypocapnic, whilst only four (30%) of the controls (13) had an arterial [Formula: see text] <4.7 kPa (P<0.001). The incidence of hypocapnic alkalosis was higher in the pregnant group (65% vs 8%; P=0.001). The CSF-to-plasma Pco2 difference was significantly higher in pregnant women (1.5 [0.3] vs 1.0 [0.4] kPa; P<0.001), mainly because of a decrease in arterial Pco2 (3.9 [0.3] vs 4.9 [0.5] kPa; P<0.001). Similarly, the CSF-to-plasma difference in SID was less negative in pregnant women (-7.8 [1.4] vs -11.4 [2.3] mM; P<0.001), mainly because of a decreased arterial SID (31.5 [1.2] vs 36.1 [1.9] mM; P<0.001). The major determinant of the reduced plasma SID of pregnant women was a relative increase in plasma chloride compared with sodium. CONCLUSIONS: Primary hypocapnic alkalosis characterises third-trimester pregnant women leading to chronic acid-base adaptations of CSF and plasma. The compensatory SID reduction, mainly sustained by an increase in chloride concentration, is more pronounced in plasma than in CSF, as the decrease in Pco2 is more marked in this compartment. CLINICAL TRIAL REGISTRATION: NCT03496311.

The incidence, hospitalisations and deaths in acutely ill children with dysnatraemias.

AIM: The aim was to evaluate the incidence, hospitalisations and deaths in acutely ill children with dysnatraemias. METHODS: This was a register-based cohort study of 46 518 acutely ill children aged <16 years who visited a paediatric emergency department. Risk factors were assessed using two nested case-control studies. RESULTS: Moderate to severe hypernatraemia occurred in 92 children (0.20%; 95% confidence interval [CI]: 0.16%-0.24%) and moderate to severe hyponatraemia in 131 children (0.28%; 95% CI: 0.24%-0.33%). Underlying medical conditions increased the risk of both moderate to severe hypernatraemia (odds ratio [OR]: 17; 95% 5.5-51) and moderate to severe hyponatraemia (OR: 3.5; 95% CI: 2.0-5.9). The use of a feeding tube (OR: 14; 95% CI: 3.2-66) and intellectual disability (OR: 7.3; 95% CI: 3.0-18) was associated with moderate to severe hypernatraemia. The risk of death was associated with moderate to severe hypernatraemia (OR: 19; 95% CI: 2.0-2564) and moderate to severe hyponatraemia (OR: 33; 95% CI: 3.7-4311). CONCLUSIONS: Severe dysnatraemias were more prevalent in acutely ill children with underlying medical conditions and were markedly associated with the risk for death.

Impact of Sodium Levels on Functional Outcomes in Patients With Stroke - A Swiss Stroke Registry Analysis.

CONTEXT: Correction of hyponatremia might represent an additional treatment for improving stroke patients' clinical outcomes. OBJECTIVE: Admission hyponatremia is associated with worse clinical outcome in stroke patients, but whether normalization of hyponatremia improves outcome is unknown. We investigated whether normalization of hyponatremia affects patients' disability, mortality, and stroke recurrence within 3 months; length of hospitalization; and discharge destination. DESIGN: This was a registry-based analysis of data collected between January 2016 and December 2018. We linked data from Swiss Stroke Registry (SSR) with electronic patients' records for extracting sodium values. SETTING: We analyzed data of hospitalized patients treated at University Hospital of Basel. PATIENTS: Stroke patients whose data and informed consent were available. MAIN OUTCOME MEASURE: Modified Rankin Scale (mRS) score at 3 months. The tested hypothesis was formulated after SSR data collection but before linkage with electronic patients' records. RESULTS: Of 1995 patients, 144 (7.2%) had hyponatremia on admission; 102 (70.8%) reached normonatremia, and 42 (29.2%) remained hyponatremic at discharge. An increase of initial sodium was associated with better functional outcome at 3 months (odds ratio [OR] 0.94; 95% CI, 0.90-0.99, for a shift to higher mRS per 1 mmol/L sodium increase). Compared with normonatremic patients, patients who remained hyponatremic at discharge had a worse functional outcome at 3 months (odds ratio 2.46; 95% CI, 1.20-5.03, for a shift to higher mRS). No effect was found on mortality, recurrence, or length of hospitalization. CONCLUSIONS: In hospitalized acute stroke patients, persistent hyponatremia is associated with worse functional outcome. Whether active correction of hyponatremia improves outcome remains to be determined in prospective studies.

Postoperative dysnatremia in infants after open-heart surgery occurs frequently and is associated with prolonged intensive care length of stay.

BACKGROUND: Dysnatremia after surgery for congenital heart disease (CHD) is well known and has been associated with prolonged pediatric intensive care unit length of stay (PICU-LOS). Fluctuations in plasma sodium levels occur perioperatively. The primary aim of the study was to evaluate the occurrence of dysnatremia during the first 48 h after surgery and whether it was associated with PICU-LOS. The secondary aim was to evaluate if the degree of sodium fluctuations was associated with PICU-LOS. METHODS: A retrospective observational, single-center study including infants undergoing surgery for CHD. The highest and lowest plasma sodium value was registered for the prespecified time periods. PICU-LOS was analyzed in relation to the occurrence of dysnatremia and the degree of plasma sodium fluctuations. The occurrence of dysnatremia was evaluated in relation to surgical procedure and fluid administration. RESULTS: Two hundred and thirty infants who underwent 249 surgical procedures were included. Dysnatremia developed in more than 60% within 48 h after surgery. Infants with normonatremia had a 40%-50% shorter PICU-LOS among children in RACHS-1 category 3-6, compared with infants developing either hypo- or hyper-/hyponatremia within 48 h after surgery (p = .006). Infants who had a decline of plasma sodium >11 mmol/L had almost double the PICU-LOS compared to those with a decline of <8 mmol/L. CONCLUSION: Dysnatremias were common after surgery for CHD and associated with prolonged PICU-LOS. The degree of decline in plasma sodium was significantly associated with PICU-LOS. Fluid administration both in terms of volume and components (blood products and crystalloids) as well as diuresis were related to the occurrence of dysnatremias.

Tonicity Matters, Especially in Complex Hyponatremia Resulting from Pseudo-, Trans-locational, and True Hypotonic Hyponatremia: An Educational Case Report.

Serum tonicity is defined by the serum concentrations of sodium (sNa) and glucose, which can promote free water movement across intra/extracellular compartments. Rapid changes in serum tonicity can cause brain damage. We herein report an educational case of a patient with hyponatremia (sNa: 112 mEq/L) concomitant with acute alcoholic pancreatitis. The cause of hyponatremia was considered complex. Pseudo- and trans-locational natremia was secondary to hyperglycemia (721 mg/dL) and hypertriglyceridemia (1,768 mg/dL), respectively, and true hypotonic hyponatremia. Regarding sNa correction, rapid correction was suspected. However, this was safely managed by monitoring tonicity (not sNa or osmolarity), thereby avoiding brain damage.

[Hypo- and hypernatremia in the intensive care unit : Pitfalls in volume management]. / Hypo- und Hypernatriämien auf der Intensivstation : Fallstricke des Volumenmanagements.

Hypo- and hypernatremias are very frequent in intensive care unit (ICU) patients and are closely related to volume disturbances and volume management in the ICU. They are associated with longer ICU stays and significant increases in mortality. Treating them is more complex than it may initially appear. Hyponatremias are differentiated based on tonicity and volume status. With hypertonic and isotonic hyponatremias, the primary focus of treatment is the underlying hyperglycemia. In case of hypotonic hypovolemic hyponatremia, the condition is treated with balanced crystalloid solutions. In eu-/hypervolemic hypotonic hyponatremias acute treatment with hypertonic saline is necessary. Hypervolemic hypernatremia occurs almost exclusively in ICU patients, often due to infusion of hypertonic solutions. There is little evidence to guide treatment, although hypotonic infusions in conjunction with diuretics may represent a legitimate approach. Great emphasis should be placed on prevention and the infusion of hypertonic solutions should be avoided. Disturbances in plasma sodium concentrations are common, requiring close attention. Exact diagnostic classification needs to be made and volume managed accordingly.

Alterações hidroeletrolíticas em pessoas com cirrose / Hydroelectrolytic alterations in cirrhotic patients

O objetivo deste estudo foi evidenciar e discutir as principais alterações hidroeletrolíticas em pessoas com cirrose. Trata-se de uma revisão integrativa, de natureza qualitativa. Os artigos foram selecionados por meio da plataforma Medical Literature Analysis and Retrievel System Online. Os principais achados identificados a partir dos artigos selecionados foram a ocorrência de hiponatremia, o mau prognóstico diante da presença de distúrbios hidroeletrolíticos em relação à sobrevida em pessoas com cirrose e a importância da albumina. Indivíduos com cirrose são suscetíveis ao desenvolvimento de distúrbios hidroeletrolíticos devido às mudanças fisiopatológicas da doença e às condições clínicas apresentadas. A hiponatremia e a hipocalemia são os mais recorrentes, destacando, porém, a necessidade de atenção aos demais distúrbios. (AU)

The objective of this study was to show and discuss the main hydroelectrolytic alterations in cirrhotic patients. This is an integrative review, a qualitative study, in which articles were selected at the Medical literature Analysis and Retrieval System Online. The main findings identified in the articles selected were the occurrence of hyponatremia, the poor prognostic, due to the presence of hydroelectrolytic disorders, regarding cirrhotic individuals survival and the importance of albumin. Individuals with cirrhosis are susceptible to the development of hydroelectrolytic disorders due to the pathophysiological alterations of the disease and because of the clinical status presented. Hyponatremia and hypokalemia are the most recurrent, but attention shall be given to the other disorders too. (AU)

Increased sodium intake and decreased sodium excretion in ICU-acquired hypernatremia: A prospective cohort study.

PURPOSE: To provide more in-depth insight in the development of early ICU-acquired hypernatremia in critically ill patients based on detailed, longitudinal and quantitative data. MATERIALS AND METHODS: A comparative analysis was performed using prospectively collected data of ICU patients. All patients requiring ICU admission for more than 48 h between April and December 2018 were included. For this study, urine samples were collected daily and analyzed for electrolytes and osmolality. Additionally, plasma osmolality analyses were performed. Further data collection consisted of routine laboratory results, detailed fluid balances and medication use. RESULTS: A total of 183 patient were included for analysis, of whom 38% developed ICU-acquired hypernatremia. Whereas the hypernatremic group was similar to the non-hypernatremic group at baseline and during the first days, hypernatremic patients had a significantly higher sodium intake on day 2 to 5, a lower urine sodium concentration on day 3 and 4 and a worse kidney function (plasma creatinine 251 versus 71.9 µmol/L on day 5). Additionally, hypernatremic patients had higher APACHE IV scores (67 versus 49, p < 0.05) and higher ICU (23 versus 12%, p = 0.07) and 90-day mortality (33 versus 14%, p < 0.01). CONCLUSIONS: Longitudinal analysis shows that the development of early ICU-acquired hypernatremia is preceded by increased sodium intake, decreased renal function and decreased sodium excretion.