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Serum lactate monitoring may help predict neurological dysfunction caused by acute metabolic crisis

Serum lactate monitoring may help predict neurological dysfunction caused by acute metabolic crisis


Neurological dysfunction can be caused by primary and secondary brain injury (caused by unstable circulation or imbalance in brain metabolic homeostasis). Elevated lactate can also be caused by the factors mentioned above. Patients with stable circulation) were excluded to minimize confounding factors.Multivariate logistic regression revealed only lactateserum and G/Lserum was independently associated with ΔGCS24hours, PaO2, Hb and MBP were not independently correlated with ΔGCS.24hours.

In this study, the results showed that postoperative serum lactate levels were higher than normal (3.7 (3.4–4.1)). A previous study showed that serum lactate was proportional to CSF ​​lactate.7 Highest correlation on the first day of ICU stay6Elevated serum lactate levels may indicate elevated intracranial lactate concentrations.

Lactic acid serum0h was above normal levels but did not correlate with ΔGCS24hours and other results, which are inconsistent with existing studies. A study of 102 gunshot patients found that serum lactate levels were negatively correlated with her GCS score on admission and positively correlated with in-hospital mortality.TenA previous study of 213 children with moderate-to-severe traumatic brain injury found that serum lactate concentrations on admission were associated with shorter mechanical ventilation, shorter ICU stay, shorter hospital stay, and It was found to be correlated with increased mortality.11A study found that serum lactate levels during surgery were not correlated with all-cause mortality, but were correlated with tumor volume.12.

Differences from existing studies are described below.

(1) various purposes Whereas existing studies have mainly focused on the predictive value of serum lactate levels in patients with acute brain injury, this study focused on the predictive value of patients under elective neurosurgery under general anesthesia. (2) different results Tumor volume or all-cause mortality was analyzed in existing studies, but focused on neurological dysfunction 24 hours after surgery. (3) Intraoperative serum lactate monitoring time for glioblastoma surgery differed in previous studies, which focused on serum lactate concentrations after tumor removal when admitted to the ICU.

Furthermore, we found that the predictive value of serum lactate increased with the extent of monitoring time.serum16h and lactic acid serum24 hours correlated with ΔGCS24hoursICU LOS, neurological complications, 28-day mortality, and 6-month GOSE (p< 0.05).Predicted value of lactateserum24 hours at ΔGCS24hours It was the best, AUROC of lactic acid bacteriaserum24 hours at ΔGCS24hours 0.85, 95% CI 0.85 to 0.93, sensitivity 75%, specificity 90.9%, cutoff 3.15.The graph of the dynamic change in serum lactate concentration shows that the serum lactate concentration of ΔGCS is24hours Decreased patients had no tendency to recover during their 24-hour ICU stay, and their ΔGCS serum lactate24hours Patients who did not decrease showed signs of recovery (Fig. Four).

We investigated the predictive value of G/L to find early indicators of neurological dysfunction.serum ratio according to existing studies.Results showed G/Lserum correlated with ΔGCS24hoursG/Lserum It had predictive value for neurological dysfunction.

It was the same or similar to existing studies.A previous study, by monitoring CSF lactate and glucose levels in TBI patients with CMD, found that CSF lactate/pyruvate and glutamate levels increased and CSF glucose decreased in patients with cerebral metabolic disorders.13A previous study monitored 89 patients with moderate-to-severe TBI continuously for 72 hours and the result was a 76% reduction in cranial extracellular glucose levels in 84 patients who received adequate fluid resuscitation. and suggested that lactate/pyruvate levels were elevated in 93%. , and 74% had a cerebral metabolic crisis14A previous study investigated 10 out-of-hospital cardiac arrest patients who underwent hypothermia and monitored CSF lactate and glucose concentrations hourly by CMD. Results showed that her lactate/pyruvate concentrations during the first 4 days after admission correlated with his Glasgow-Pittsburgh brain performance categories 30 days after his cardiac arrest, whereas glucose It was found to be correlated with the outcome of15In one study, by examining data from 1873 cases, >30 lactate/pyruvate was associated with low cerebral perfusion pressure (CPP) but not with increased intracranial pressure (ICP). was suggested.16.

G/Lserum was found with predictive values ​​for 28-day mortality and 6-month GOSE, but may not provide a valuable reference for the prediction of neurological complications. This result was obtained for the following reasons. Most of the neurological complications in this study included delirium and agitation, mild neurological dysfunctions that are difficult to assess and distinguish by GCS score.17Because the above neurological complications were transient and most patients were able to recover during the 24-hour ICU stay, the GCS score after 24-hour ICU stay may not indicate the above complications. I have. As a result, G/Lserum It may not provide a valuable reference for prediction of neurological complications.

As mentioned above, the increase in serum lactate level is thought to reflect the increase in brain lactate concentration, and neuronal dysfunction in this study was associated with brain metabolic factors. ) were excluded before analysis. Lactic acid is an important metabolic substrate in the brain, and it has been confirmed that when the energy consumption balance of the brain is disturbed, the concentrations of lactate and glucose in the brain change to similar levels, resulting in a state of low glucose and high lactate concentrations. increase.called acute metabolic crisis (ACMC)18ACMC can arise from primary brain injury and is recognized as the etiology of secondary brain injury, causing acute neurological dysfunction and affecting long-term outcome. A study of 14 TBI patients with 1-year follow-up found that ACMC caused atrophy of the frontal and parietal lobes, resulting in varying degrees of impairment in attention, executive performance, cognitive performance, and affective deficits. was shown.19A study of TBI patients confirmed a correlation between the cerebrospinal fluid (CSF) glucose/lactate ratio and ACMC.20.

Looking back at the results, postoperative serum lactate levels are generally higher than normal, which may reflect an increase in intracranial lactate concentration, a phenomenon commonly present in ACMC after surgery, It has been clarified that conversion and mobilization of energy substrates are carried out. Cellular levels increased with increasing energy demand. ΔGCS serum lactate24hours Decreased patients had no tendency to recover during their 24-hour ICU stay, and their ΔGCS serum lactate24hours Patients who did not decrease tended to recover (Fig. Four), consistent hyperlactatemia mirrored consistent ACMC, and consistent ACMC caused brain homeostatic imbalance and neuronal dysfunction. turned out to be twenty oneif adequate sedation and analgesia could be implemented after neurosurgery, ACMC would probably not occur and neuropathy would be reduced.




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