Sodium lactate 9.25g/500ml infusion bags

BACKGROUND: Sodium lactate–based solutions have been proposed as an alternative to conventional osmotic therapies for intracranial pressure (ICP) control in acute brain injury (ABI). Beyond their osmotic properties, lactate may also act as a cerebral metabolic substrate, although its effects appear context-dependent. The aim of this systematic review was to synthesize available data on lactate-based therapies in ABI, focusing on their effects on intracranial dynamics, cerebral metabolism and neurological outcomes to guide future clinical translation. METHODS: We performed a systematic review of preclinical and clinical studies evaluating exogenous sodium lactate administration in ABI, including traumatic brain injury, ischemic stroke, and cardiac arrest. Outcomes of interest included intracranial pressure control, cerebral metabolism, cerebral perfusion and oxygenation, systemic hemodynamics, safety, and functional recovery. RESULTS: Twelve preclinical and twelve clinical studies were included. Across most models, sodium lactate was effective in reducing ICP and at least as effective and safe as mannitol or hypertonic saline in clinical settings. Several studies reported improved systemic hemodynamic tolerance compared with conventional osmotherapy. Preclinical and clinical metabolic data demonstrated that lactate can be taken up and oxidized by the injured brain; however, metabolic benefits were inconsistent and appeared dependent on preserved oxidative metabolism, baseline metabolic status, timing, and dose. Functional outcome data were limited but suggested potential cognitive and neurological benefits in both experimental and selected clinical settings. CONCLUSIONS: Sodium lactate is an effective therapy for intracranial hypertension and may offer additional metabolic and systemic advantages in ABI patients under specific conditions. Its metabolic effects appear critically dependent on preserved oxidative capacity, highlighting the need for improved patient selection and the potential role of metabolic monitoring to guide therapy. The impact of lactate-based treatments on meaningful functional outcomes remains uncertain and warrants further investigation in targeted clinical trials.

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BackgroundTwo randomized trials (BICAR-ICU and BICAR-ICU2) evaluated intravenous sodium bicarbonate therapy in patients with severe metabolic acidemia but yielded inconclusive results. We performed an individual patient data meta-analysis to assess its effects on 90-day mortality and renal replacement therapy (RRT) use, and search for heterogeneity of treatment effects across prespecified subgroups.MethodsWe performed an individual patient data meta-analysis of the BICAR-ICU and BICAR-ICU2 trials, including adults with severe metabolic acidemia (pH ≤ 7.20). Patients were randomized to receive intravenous sodium bicarbonate titrated to a pH ≥ 7.30 or no sodium bicarbonate. The primary outcome was 90-day mortality. Secondary outcomes included RRT initiation and dialysis-free days. Prespecified subgroup analyses explored treatment-effect heterogeneity by acidemia depth (pH ≤ 7.10 vs. > 7.10), severe acute kidney injury (AKI) status, and serum lactate (ResultsA total of 1,016 patients was included (509 sodium bicarbonate, 507 control). Sodium bicarbonate therapy did not significantly reduce 90-day mortality compared to control (58.3% vs. 60.6%; risk ratio [RR], 0.96; 95%CI, 0.86-1.07; p = 0.51). However, it significantly reduced RRT initiation (34.8% vs. 50.7%; RR, 0.69; 95%CI, 0.60-0.79; p  7.10 (RR, 1.05; 95%CI, 0.92-1.21; p = 0.47). No significant interactions were observed for severe AKI status (p-for-interaction = 0.11) nor serum lactate (p-for-interaction = 0.22).ConclusionsSodium bicarbonate therapy did not reduce overall 90-day mortality but decreased RRT use and suggested a mortality benefit in patients with the most profound acidemia (pH ≤ 7.10). These findings invite a reconsideration of current paradigms, suggesting timely correction of severe metabolic acidemia to avoid RRT in some patients.

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PurposeHypertonic fluids such as mannitol and half-molar sodium lactate are given to treat intracranial hypertension in patients with severe traumatic brain injury (TBI). In this study, sodium lactate was compared to mannitol in patients with TBI to investigate the efficacy in reducing intracranial pressure (ICP).MethodsThis study was a systematic review with literature research on articles published in any year in the databases of PubMed, ScienceDirect, Asian Journal of Neurosurgery, and Cochrane Central Register of Controlled Trials. The keywords were "half-molar sodium lactate", "mannitol", "cerebral edema or brain swelling", and "severe traumatic brain injury". The inclusion criteria were (1) studies published in English, (2) randomized control trials or retrospective/prospective studies on TBI patients, and (3) therapies including half-molar sodium lactate and mannitol and (4) sufficient data such as mean difference (MD) and risk ratio (RR). Data analysis was conducted using Review Manager 5.3.ResultsFrom 1499 studies, a total of 8 studies were eligible. Mannitol group reduced ICP of 0.65 times (MD 0.65; p = 0.64) and improved cerebral perfusion pressure of 0.61 times (MD 0.61; p = 0.88), better than the half-molar group of sodium lactate. But the half-molar group of sodium lactate maintained the mean arterial pressure level of 0.86 times, better than the mannitol group (MD 0.86; p = 0.09).ConclusionHalf-molar sodium lactate is as effective as mannitol in reducing ICP in the early phase of brain injury, superior over mannitol in an extended period. It is able to prevent intracranial hypertension and give better brain tissue perfusion as well as more stable hemodynamics. Blood osmolarity is a concern as it increases serum sodium.

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BackgroundIntravenous fluid therapy represents the most common intervention critically ill patients are exposed to. Hyperchloremia and metabolic acidosis associated with 0.9% sodium chloride have been observed to lead to worse outcomes, including mortality. Balanced solutions, such as Plasma-Lyte 148 and Compound Sodium Lactate, represent potential alternatives but the evidence on optimal fluid choices in critically ill children remains scarce. This study aims to demonstrate whether balanced solutions, when used as intravenous fluid therapy, are able to reduce the incidence of a rise in serum chloride level compared to 0.9% sodium chloride in critically ill children.MethodsThis is a single-centre, open-label randomized controlled trial with parallel 1:1:1 assignment into three groups: 0.9% sodium chloride, Plasma-Lyte 148, and Compound Sodium Lactate solutions for intravenous fluid therapy. The intervention includes both maintenance and bolus fluid therapy. Children aged DiscussionThis study tests three types of intravenous fluid therapy in order to compare the risk of hyperchloremia associated with normal saline versus balanced solutions. This pragmatic study is thereby assessing the most common intervention in paediatric critical care. This is a single-centre open-label study with no blinding at the level of delivery of the intervention. Certain paediatric intensive care unit (PICU) patient groups such as those admitted with a cardiac condition or following a traumatic brain injury are excluded from this study.Trial registrationThe study has received ethical approval (HREC/19/QCHQ/53177: 06/06/2019). It is registered in the Australian New Zealand Clinical Trials Registry ( ACTRN12619001244190 ) from 9th September 2019. Recruitment commenced on 12th November 2019. The primary results manuscript will be published in a peer-reviewed journal.

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