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Risk Factors and Outcomes of Rapid Correction of Severe Hyponatremia.

ABSTRACT: BACKGROUND AND OBJECTIVES:Rapid correction of severe hyponatremia can result in serious neurologic complications, including osmotic demyelination. Few data exist on incidence and risk factors of rapid correction or osmotic demyelination. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS:In a retrospective cohort of 1490 patients admitted with serum sodium <120 mEq/L to seven hospitals in the Geisinger Health System from 2001 to 2017, we examined the incidence and risk factors of rapid correction and osmotic demyelination. Rapid correction was defined as serum sodium increase of >8 mEq/L at 24 hours. Osmotic demyelination was determined by manual chart review of all available brain magnetic resonance imaging reports. RESULTS:Mean age was 66 years old (SD=15), 55% were women, and 67% had prior hyponatremia (last outpatient sodium <135 mEq/L). Median change in serum sodium at 24 hours was 6.8 mEq/L (interquartile range, 3.4-10.2), and 606 patients (41%) had rapid correction at 24 hours. Younger age, being a woman, schizophrenia, lower Charlson comorbidity index, lower presentation serum sodium, and urine sodium <30 mEq/L were associated with greater risk of rapid correction. Prior hyponatremia, outpatient aldosterone antagonist use, and treatment at an academic center were associated with lower risk of rapid correction. A total of 295 (20%) patients underwent brain magnetic resonance imaging on or after admission, with nine (0.6%) patients showing radiologic evidence of osmotic demyelination. Eight (0.5%) patients had incident osmotic demyelination, of whom five (63%) had beer potomania, five (63%) had hypokalemia, and seven (88%) had sodium increase >8 mEq/L over a 24-hour period before magnetic resonance imaging. Five patients with osmotic demyelination had apparent neurologic recovery. CONCLUSIONS:Among patients presenting with severe hyponatremia, rapid correction occurred in 41%; nearly all patients with incident osmotic demyelination had a documented episode of rapid correction. PODCAST:This article contains a podcast at https://www.asn-online.org/media/podcast/CJASN/2018_06_05_CJASNPodcast_18_7_G.mp3.

SUBMITTER: George JC

PROVIDER: S-EPMC6032596 | biostudies-literature | 2018 Jul

REPOSITORIES: biostudies-literature

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Risk Factors and Outcomes of Rapid Correction of Severe Hyponatremia.

George Jason C JC Zafar Waleed W Bucaloiu Ion Dan ID Chang Alex R AR

Clinical journal of the American Society of Nephrology : CJASN 20180605 7

<h4>Background and objectives</h4>Rapid correction of severe hyponatremia can result in serious neurologic complications, including osmotic demyelination. Few data exist on incidence and risk factors of rapid correction or osmotic demyelination.<h4>Design, setting, participants, & measurements</h4>In a retrospective cohort of 1490 patients admitted with serum sodium <120 mEq/L to seven hospitals in the Geisinger Health System from 2001 to 2017, we examined the incidence and risk factors of rapid ...[more]

PMID: 29871886

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Project description:Background and objectivesOsmotic demyelination syndrome is the most concerning complication of severe hyponatremia, occurring with an overly rapid rate of serum sodium correction. There are limited clinical tools to aid in identifying individuals at high risk of overcorrection with severe hyponatremia.Design, setting, participants, & measurementsWe identified all patients who presented to a tertiary-care hospital emergency department in Ottawa, Canada (catchment area 1.2 million) between January 1, 2003 and December 31, 2015, with serum sodium (corrected for glucose levels) <116 mmol/L. Overcorrection was determined using 14 published criteria. Latent class analysis measured the independent association of baseline factors with a consensus overcorrection status on the basis of the 14 criteria, and was summarized as a risk score, which was validated in two cohorts.ResultsA total of 623 patients presented with severe hyponatremia (mean initial value 112 mmol/L; SD 3.2). The prevalence of no, unlikely, possible, and definite overcorrection was 72%, 4%, 10%, and 14%, respectively. Overcorrection was independently associated with decreased level of consciousness (2 points), vomiting (2 points), severe hypokalemia (1 point), hypotonic urine (4 points), volume overload (-5 points), chest tumor (-5 points), patient age (-1 point per decade, over 50 years), and initial sodium level (<110 mmol/L: 4 points; 110-111 mmol/L: 2 points; 112-113 mmol/L: 1 point). These points were summed to create the Severe Hyponatremic Overcorrection Risk (SHOR) score, which was significantly associated with overcorrection status (Spearman correlation 0.45; 95% confidence interval, 0.36 to 0.49) and was discriminating (average dichotomized c-statistic 0.77; 95% confidence interval, 0.73 to 0.81). The internal (n=119) and external (n=95) validation cohorts had significantly greater use of desmopressin, which was significantly associated with the SHOR score. The SHOR score was significantly associated with overcorrection status in the internal (P<0.001) but not external (P=0.39) validation cohort.ConclusionsIn patients presenting with severe hyponatremia, overcorrection was common and predictable using baseline information. Further external validation of the SHOR is required before generalized use.

Project description:Micronutrient deficiencies and environmental exposures have been to known to adversely impact brain and nervous system functions in adults and children worldwide. However, few studies have examined the short and long-term impact of these risk factors on neurodevelopmental outcomes in children in low-income countries, where the effects are likely to be more pronounced due to limited resources for monitoring and insufficient regulations. Biological risk factors of relevance include micronutrient deficiencies such as zinc and exposure to heavy metals such as lead and mercury. Studies have suggested an association between neurodevelopmental impairment and micronutrient deficiency as well as exposure to a number of heavy metals and environmental toxins. Moreover, findings also suggest that risk factors for adverse developmental outcomes that are independently significant may have the potential for causing cumulative increases in adverse effects. In Sub-Saharan Africa, severe malaria is a leading risk factor for long-term neurocognitive impairment in children. Zinc deficiency or exposure to heavy metals could influence risk of severe malaria, modify the risk of neurocognitive impairment in children with severe malaria, or independently affect risk of neurocognitive impairment. Untargeted analyses for potential environmental exposures or metabolomic changes in children with cerebral malaria vs. without cognitive impairment or in children with higher vs. lower cognitive scores, could also identify new risk factors for neurodevelopmental impairment in Ugandan children with cerebral malaria.In our completed study in Kampala, we assessed neurologic and developmental impairment in children with cerebral malaria [CM] or severe malarial anemia [SMA], as compared to health community children from the same extended household as the children with CM or SMA. As an extension of this study, we are interested in determining levels of micronutrients such as zinc in the population, and in addition, determining exposure levels of heavy metals (lead, mercury, copper, manganese etc.) in samples collected from children with severe malaria and community controls. The primary hypotheses of this study is that nutrient deficiencies or exposure to heavy metals influence short and long term neurocognitive outcomes in healthy community children and in children with severe malaria, and that children with cerebral malaria have specific metabolomic changes that relate to long-term neurocognitive impairment. The specific aims of our study are:Aim 1: To determine levels of zinc, heavy metals, and biomarkers associated with inflammation in children presenting with different forms of severe malaria (SM) and in healthy community children (CC). The working hypothesis of this aim is that 1) children with SM will have lower zinc levels compared to CC; 2) children with SM will present with higher toxic metal exposure and higher levels of biomarkers associated with inflammation than CC.Aim 2: To investigate how micronutrient deficiency, toxic metal exposure and inflammatory biomarkers affect short and long term neurodevelopmental outcomes and growth in children with severe malaria and community children (CC).The working hypothesis of this aim is that the lower levels of zinc, and presence of toxic metals in high concentrations will independently contribute to worsening neurodevelopmental outcomes and worsening growth over time in children with severe malaria and in community children. An alternate hypothesis is that micronutrient deficiency, toxic metal exposure and inflammatory states may interact with each other and with severe malaria to produce greater neurodevelopmental impairment, i.e., that the contribution is not independent but interactive.Aim 3: To determine whether the CSF metabolome differs according to level of neurodevelopmental impairment in children with cerebral malaria. The working hypothesis of this aim is that neurodevelopmental impairment in children with cerebral malaria is associated with changes in the CSF metabolome.

Project description:BackgroundCOVID-19 is a multisystemic disorder that frequently causes acute kidney injury (AKI). However, the precise clinical and biochemical variables associated with AKI progression in patients with severe COVID-19 remain unclear.MethodsWe performed a retrospective study on 278 hospitalized patients who were admitted to the ward and intensive care unit (ICU) with COVID-19 between March 2020 and June 2020, at the University Hospital, São Paulo, Brazil. Patients aged ≥ 18 years with COVID-19 confirmed on RT-PCR were included. AKI was defined according to the Kidney Disease Improving Global Outcomes (KDIGO) criteria. We evaluated the incidence of AKI, several clinical variables, medicines used, and outcomes in two sub-groups: COVID-19 patients with AKI (Cov-AKI), and COVID-19 patients without AKI (non-AKI). Univariate and multivariate analyses were performed.ResultsFirst, an elevated incidence of AKI (71.2%) was identified, distributed across different stages of the KDIGO criteria. We further observed higher levels of creatinine, C-reactive protein (CRP), leukocytes, neutrophils, monocytes, and neutrophil-to-lymphocyte ratio (NLR) in the Cov-AKI group than in the non-AKI group, at hospital admission. On univariate analysis, Cov-AKI was associated with older age (>62 years), hypertension, CRP, MCV, leucocytes, neutrophils, NLR, combined hydroxychloroquine and azithromycin treatment, use of mechanical ventilation, and vasoactive drugs. Multivariate analysis showed that hypertension and the use of vasoactive drugs were independently associated with a risk of higher AKI in COVID-19 patients. Finally, we preferentially found an altered erythrocyte and leukocyte cellular profile in the Cov-AKI group compared to the non-AKI group, at hospital discharge.ConclusionsIn our study, the development of AKI in patients with severe COVID-19 was related to inflammatory blood markers and therapy with hydroxychloroquine/azithromycin, with vasopressor requirement and hypertension considered potential risk factors. Thus, attention to the protocol, hypertension, and some blood markers may help assist doctors with decision-making for the management of COVID-19 patients with AKI.

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Risk Factors and Outcomes of Rapid Correction of Severe Hyponatremia.

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Risk Factors and Outcomes of Rapid Correction of Severe Hyponatremia.

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