Hypertonic saline in critical illness - A systematic review

Pfortmueller, Carmen A.; Schefold, Joerg C.

doi:10.1016/j.jcrc.2017.06.019

Cited by 31 publications

(38 citation statements)

References 74 publications

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“…Due to the retrospective fashion of this analysis, preoperative baseline characteristics of BE and lactate-levels were not available. Last, neither chloride-levels nor fluid intake, which both impact on the metabolic status of respective patients [ 8 , 15 , 23 , 38 ], were recorded, therefore a hyperchloraemic acidosis and/or dilutional acidosis in respective patients cannot be excluded with certainty.…”

Section: Discussionmentioning

confidence: 99%

Base excess is superior to lactate-levels in prediction of ICU mortality after cardiac surgery

Zante

Reichenspurner²,

Kubik

et al. 2018

PLoS ONE

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IntroductionCardiac surgery with the use of cardiopulmonary bypass is known to induce distinct metabolic changes. Respective changes in acid-base status including increased systemic lactate levels were previously related to clinical outcomes, but data remain controversial. Therefore, we aim to investigate the relevance of lactate and base excess (BE) levels on ICU-mortality in patients admitted to the ICU after cardiac surgery.Materials and methodsPerioperative data of patients treated in a tertiary care academic center admitted to the ICU after on-pump surgery were analyzed in a retrospective fashion. Receiver operation characteristic (ROC) curves were constructed for admission lactate-levels and BE with calculation of optimal cut-off values to predict ICU mortality. Univariate followed by multivariate regression models were constructed to identify potential outcome-relevant indices.ResultsData from 1,058 patients were included in the analysis. Area under the curves for prediction of ICU mortality were 0.79 for lactate levels at ICU admission (sensitivity 61.9%/ specificity 87.5%; optimal cut-off level 3.9mmol/l), and 0.7 for BE (sensitivity 52.4%/ specificity 93.8%, optimal cut-off level -6.7), respectively. Multivariate regression identified BE < -6.7 as the single metabolic predictor of ICU-mortality (HR 4.78, 95%-CI 1.4–16.33, p = 0.01). Explorative subgroup analyses revealed that the combination of lactate ≤3.9mmol/l and BE ≤ -6.7 has stronger impact on mortality than a combination of lactate of >3.9mmol/l and BE > -6.7 (HR 2.56, 95%-CI 0.18–37.17).ConclusionsAt ICU-admission, severely reduced BE appears superior to hyperlactatemia with regard to prediction of ICU-mortality in patients after cardiac surgery.

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Section: Discussionmentioning

confidence: 99%

Base excess is superior to lactate-levels in prediction of ICU mortality after cardiac surgery

Zante

Reichenspurner²,

Kubik

et al. 2018

PLoS ONE

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“…Hyperchloremia in critical illness most often results from iatrogenic chloride overload (e.g., 0.9% NaCl infusion with 154 mmol/l CL − ) [ 1 , 12 , 27 – 30 ]. Normal saline has a theoretical SID of zero [ 1 ] and thus results in development of hyperchloremic metabolic acidosis [ 1 , 12 ].…”

Section: Reviewmentioning

confidence: 99%

“…Normal saline has a theoretical SID of zero [ 1 ] and thus results in development of hyperchloremic metabolic acidosis [ 1 , 12 ]. Despite growing evidence, 0.9% NaCl is still one of the most widely used crystalloids [ 12 , 30 – 36 ]; however, its use is widely debated [ 37 – 43 ]. Importantly, the ICU physician should note that albumin-based replacement fluids may contain rather large quantities of chloride also [ 44 , 45 ].…”

Section: Reviewmentioning

confidence: 99%

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Serum chloride levels in critical illness—the hidden story

Pfortmueller

Uehlinger

Haehling

et al. 2018

ICMx

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Chloride is the principal anion of the extracellular fluid and vital for both serum electroneutrality and acid-base homeostasis. The aim of this review is to investigate the relevance of dyschloremia in the critically ill.An extensive literature research was conducted on www.pubmed.org. In addition, the references of included articles were searched for further possible investigation regarding chloride.Articles investigating the relevance of dyschloremia in the critically ill were included.All articles were screened in regard to dyschloremia in the critically ill.Chloride is essential for blood pressure control, decarboxylation/gas transport, renal function, and gastrointestinal homeostasis. “Dyschloremia,” i.e., serum chloride levels not within the limits of normal, may commonly be observed on ICUs and appear mainly induced by iatrogenic measures (i.e., infusion of chloride-rich fluids). Hypo- and hyperchloremia appear linked to increased mortality in defined ICU populations, but evidence is sparse. Data show that hyperchloremia may not only be linked to hyperchloremic metabolic acidosis, but also to increased hemodynamic instability and vasopressor need (e.g., in patients after major surgery). Nevertheless, it is currently unknown whether such effects would be directly or indirectly mediated. Moreover, recent evidence points to an increased incidence of acute kidney injury and need for renal replacement therapy in patients with advanced hyperchloremia.Current knowledge on chloride is largely limited by heterogeneous trial design and mostly abundant data on specific fluid replacement strategies. The aim of this review is to summarize key consequences of chloride in critical illness and to discuss implications for daily clinical practice and future research.

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“…Hypertonic saline has additional, potentially beneficial effects beyond its role in mitigating cerebral edema. Hypertonic saline, when administered, can improve mean arterial pressure, cardiac output, and stroke volume, potentially lifesaving in traumatic injuries or septic shock [55,61]. Up until this point, there have been small randomized clinical trials demonstrating the beneficial effects of hypertonic saline in the management of cerebral edema; however, the demonstration of improvement in patient outcome had remained elusive.…”

Section: Osmolar Therapiesmentioning

confidence: 99%

The Medical Management of Cerebral Edema: Past, Present, and Future Therapies

Halstead

Geocadin

2019

Neurotherapeutics

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Cerebral edema is commonly associated with cerebral pathology, and the clinical manifestation is largely related to the underlying lesioned tissue. Brain edema usually amplifies the dysfunction of the lesioned tissue and the burden of cerebral edema correlates with increased morbidity and mortality across diseases. Our modern-day approach to the medical management of cerebral edema has largely revolved around, an increasingly artificial distinction between cytotoxic and vasogenic cerebral edema. These nontargeted interventions such as hyperosmolar agents and sedation have been the mainstay in clinical practice and offer noneloquent solutions to a dire problem. Our current understanding of the underlying molecular mechanisms driving cerebral edema is becoming much more advanced, with differences being identified across diseases and populations. As our understanding of the underlying molecular mechanisms in neuronal injury continues to expand, so too is the list of targeted therapies in the pipeline. Here we present a brief review of the molecular mechanisms driving cerebral edema and a current overview of our understanding of the molecular targets being investigated.

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Hypertonic saline in critical illness - A systematic review

Cited by 31 publications

References 74 publications

Base excess is superior to lactate-levels in prediction of ICU mortality after cardiac surgery

Base excess is superior to lactate-levels in prediction of ICU mortality after cardiac surgery

Serum chloride levels in critical illness—the hidden story

The Medical Management of Cerebral Edema: Past, Present, and Future Therapies

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