sodium-lactate and Brain-Injuries

Preventive treatments of traumatic intracranial hypertension are not yet established. We aimed to compare the efficiency of half-molar sodium lactate (SL) versus saline serum solutions in preventing episodes of raised intracranial pressure (ICP) in patients with severe traumatic brain injury (TBI).. This was a double-blind, randomized controlled trial including 60 patients with severe TBI requiring ICP monitoring. Patients were randomly allocated to receive a 48-h continuous infusion at 0.5 ml/kg/h of either SL (SL group) or isotonic saline solution (control group) within the first 12 h post-trauma. Serial measurements of ICP, as well as fluid, sodium, and chloride balance were performed over the 48-h study period. The primary outcome was the number of raised ICP (≥20 mmHg) requiring a specific treatment.. Raised ICP episodes were reduced in the SL group as compared to the control group within the 48-h study period: 23 versus 53 episodes, respectively (p < 0.05). The proportion of patients presenting raised ICP episodes was smaller in the SL group than in the saline group: 11 (36 %) versus 20 patients (66 %) (p < 0.05). Cumulative 48-h fluid and chloride balances were reduced in the SL group compared to the control group (both p < 0.01).. A 48-h infusion of SL decreased the occurrence of raised ICP episodes in patients with severe TBI, while reducing fluid and chloride balances. These findings suggest that SL solution could be considered as an alternative treatment to prevent raised ICP following severe TBI.

Topics: Adolescent; Adult; Aged; Body Fluids; Brain Injuries; Chlorides; Double-Blind Method; Female; Humans; Infusions, Intravenous; Injury Severity Score; Intracranial Hypertension; Male; Middle Aged; Prospective Studies; Sodium; Sodium Lactate; Young Adult

Traumatic brain injury (TBI) is still a major cause of mortality and morbidity. Recent trials have failed to demonstrate a beneficial outcome from therapeutic treatments such as corticosteroids, hypothermia and hypertonic saline. We investigated the effect of a new hyperosmolar solution based on sodium lactate in controlling raised intracranial pressure (ICP).. Prospective open randomized study in an adult ICU.. Thirty-four patients with isolated severe TBI (Glasgow Coma Scale

Topics: Adult; Brain Edema; Brain Injuries; Disability Evaluation; Diuretics, Osmotic; Female; Glasgow Coma Scale; Humans; Injury Severity Score; Intensive Care Units; Intracranial Hypertension; Male; Mannitol; Prospective Studies; Sodium Lactate

Intracranial hypertension (ICH) is the most important modifiable factor with predictive negative value in brain injury patients. Osmotherapy is the most important first level specific measure in the treatment of ICH. Mannitol 20%, and 3, 7.5, 10, and 23% hypertonic sodium chloride are the most commonly used osmotic agents in the neurocritical care setting. Currently, controversy about the best osmotic agent remains elusive. Therefore, over the past few years, half-molar sodium lactate has been introduced as a new osmotic agent to be administered in the critically ill. Lactate is able to prevent hyperchloremia, as well as its adverse effects such as hyperchloremic acidosis, systemic inflammation, and acute kidney injury. Furthermore, lactate may also be used by glia as energy substrate in brain injury patients. Half-molar sodium lactate would also have a more potent and long-lasting effect decreasing intracellular osmolarity and by inhibiting neuronal volume control mechanisms. Pioneering researches in patients with traumatic brain injury have shown a more significant effect than mannitol on the control of ICH. In addition, in this group of patients this solution appears to be beneficial in preventing episodes of ICH. However, future research is necessary to corroborate or not these promising results.

Topics: Brain Injuries; Humans; Intracranial Hypertension; Mannitol; Sodium; Sodium Lactate

Lactate has been identified as an alternative fuel for the brain in situations of increased energy demand, as following a traumatic brain injury (TBI). This study investigates the effect of treatment with sodium lactate (NaLac) on the changes in brain energy state induced by a severe diffuse TBI. Rats were assigned to one of the eight groups (n=10 per group): 1-sham, normal saline; 2-TBI, normal saline; 3-TBI, hypertonic saline; 4-TBI, 100mM NaLac, 5-TBI, 500 mM NaLac; 6-TBI, 1280 mM NaLac; 7-TBI, 2000 mM NaLac and 8-TBI-500 mM NaLac+magnesium sulfate. Cerebrums were removed 6h after trauma. Metabolites representative of the energy state (ATP, ATP-catabolites), N-acetylaspartate (NAA), antioxidant defenses (ascorbic acid, glutathione), markers of oxidative stress (malondialdehyde, ADP-ribose) and nicotinic coenzymes (NAD(+)) were measured by HPLC. TBI induced a marked decrease in the cerebral levels of ATP, NAA, ascorbic acid, glutathione and NAD(+) and a significant rise in the content of ATP-catabolites, malondialdehyde and ADP-ribose. These alterations were not ameliorated with NaLac infusion. We observed a significant reduction in cerebral NAD(+), an essential co-enzyme for mitochondrial lactate-dehydrogenase that converts lactate into pyruvate and thus replenishes the tricarboxylic acid cycle. These results suggest that the metabolic pathway necessary to consume lactate may be compromised following a severe diffuse TBI in rats.

Topics: Adenosine Triphosphate; Animals; Ascorbic Acid; Aspartic Acid; Blood Gas Analysis; Blood Pressure; Brain Chemistry; Brain Injuries; Cerebral Cortex; Chromatography, High Pressure Liquid; Disease Models, Animal; Energy Metabolism; Glutathione; Male; Models, Biological; NAD; Neuroprotective Agents; Rats; Rats, Sprague-Dawley; Sodium Lactate