Serum neuron-specific enolase levels at presentation and long-term neurological sequelae after acute charcoal burning-induced carbon monoxide poisoning

Objective: This study aimed to investigate whether clinical parameters and serum neuron-specific enolase (NSE) levels measured at emergency department (ED) presentation help stratify the risk of acute or delayed persistent severe neurological sequelae after acute carbon monoxide (CO) poisoning induced by charcoal burning.

Methods: This retrospective study included 236 patients who suffered from CO poisoning. Demographic information, serum NSE levels measured in the ED, treatment, clinical course, and long-term neurological outcomes were recorded.

Results: The median serum NSE level at presentation was 15.5 (10.9–22.7) ng/mL. No differences were observed in the duration of CO exposure; the initial Glasgow Coma Scale (GCS) score; the levels of arterial HCO₃^?, white blood cells (WBCs), C-reactive protein (CRP) or troponin I; or the frequency of abnormal diffusion-weighted imaging finding at presentation among the groups with different serum NSE levels at presentation. The incidences of acute and delayed persistent neurologic sequelae assessed at 22.3 months after acute charcoal CO poisoning were 5.1% and 8.5%, respectively. No difference in the NSE level was observed between patients stratified according to long-term neurological status. According to the multinomial logistic regression analysis, age, serum CRP levels and the initial GCS score were risk factors for the two types of persistent severe neurological sequelae, whereas troponin I levels were associated only with the acute persistent severe neurological sequelae. However, the adjusted NSE level was not a risk factor for any persistent neurological sequelae.

Conclusions: Serum NSE levels at presentation were not correlated with the risk of acute or delayed persistent neurological sequelae. Further studies with blood sampling at optimal time points and serial measurements should be conducted. Age, initial GCS score, and CRP levels may be risk factors for persistent severe neurological sequelae.     

Two Cases of Acute Carbon Monoxide Poisoning with Delayed Neurological Sequelae After a “Free” Interval

Abstract

Two cases are presented to illustrate the delayed neurological complications which may follow carbon monoxide (CO) poisoning, the mechanisms of which are not well known and which do not seem to be recognized widely enough to safeguard patients. Broad discussion is needed to determine how cases of CO exposure/poisoning should best be handled if sequelae are to be avoided.     

Predictive factors for acute brain lesions on magnetic resonance imaging in acute carbon monoxide poisoning

BackgroundAcute brain lesions on diffusion-weighted-magnetic resonance imaging (MRI) after acute carbon monoxide (CO) poisoning were associated with delayed neurological sequelae. This study was conducted to identify the risk factors associated with acute brain lesions on MRI after acute CO poisoning and to help select patients who need acute-phase brain MRI after acute CO poisoning in the emergency department (ED).MethodsThis retrospective observational study included 103 adult patients who were hospitalized at a tertiary-care hospital between November 2016 and September 2019 and underwent brain MRI because of acute CO poisoning. Multivariable logistic regression analysis was applied to identify predictive factors for acute brain lesions on MRI after acute CO poisoning.ResultsMultivariable logistic regression analysis showed that Glasgow Coma Scale (GCS) score of <9 at ED presentation (odds ratio [OR] 17.749, 95% confidence interval [CI] 3.098–101.690, P = 0.001) and the initial troponin-I level at presentation in the ED (OR 13.657, 95% CI 1.415–131.834, P = 0.024) were predictive factors for acute brain lesions on MRI in acute CO poisoning. The receiver operating characteristics curve for initial troponin-I showed an area under the curve of 0.761 (95% CI 0.638–0.883, P < 0.001) and the optimal cutoff value was 0.105 ng/mL.ConclusionsAcute-phase brain MRI in acute CO poisoning can be considered for patients who present at the ED with a GCS score <9 or troponin-I level >0.105 ng/mL.     

Prognostic value of S100B protein in carbon monoxide-poisoned rats

OBJECTIVE: To assess the possible role of S100B, a structural protein of astroglial cells, as a biochemical marker in acute carbon monoxide-poisoned rats and to compare its prognostic value with consciousness level, which is one of the major parameters for treatment decision in acute carbon monoxide poisoning. DESIGN: Nonrandomized, controlled interventional trial. SETTING: University laboratory. SUBJECTS: Male Wistar rats weighing 263 +/- 18 g. INTERVENTIONS: The rats were exposed to a mixture of 3000 ppm carbon monoxide in air for 60 mins (group 1) and a mixture of 5000 ppm carbon monoxide in air for 30 mins (group 2). Blood samples were taken from the jugular vein just before and immediately after the carbon monoxide poisoning. The level of consciousness was evaluated at the end of the exposure, and the survival rate was monitored for 7 days. The S100B concentrations were measured with a commercial immunoluminometric assay. MEASUREMENTS AND MAIN RESULTS: In the first group, the unconscious rats after carbon monoxide exposure had significantly higher S100B levels compared with the rats without loss of consciousness. In the second group, the unconscious rats that later died had significantly higher S100B levels compared with the unconscious rats that survived. The S100B levels of all conscious and unconscious surviving rats were not significantly different. The serum level of S100B below 0.44 microg/L predicted survival of carbon monoxide-poisoned rats, with a sensitivity of 100% and a specificity of 86%. CONCLUSIONS: Acute carbon monoxide poisoning is associated with elevated S100B levels. S100B is a better predictor of final outcome than the consciousness level, so it could be used as a prognostic parameter for acute carbon monoxide poisoning in rats.     

Elevated serum S100B protein and neuron-specific enolase levels in carbon monoxide poisoning

Objective

Carbon monoxide (CO) poisoning causes cerebral and generalized hypoxia. This study aimed to assess the possible use of serum glial marker S100B protein and neuron-specific enolase (NSE) as biochemical markers of hypoxic brain damage in acute CO poisoning.

Methods

Patients with acute CO poisoning admitted to the ED of 2 training hospitals (Ankara, Turkey) were included in this cross-sectional study. Serum levels of S100B and NSE were measured on admission. The patients were divided into 2 groups (unconscious and conscious). Twenty healthy adults were included in the study to serve as controls.

Results

A total of 70 patients poisoned by CO (mean age ± SD, 36.6 ± 16.3 years; 64.3% women) were enrolled. Although S100B concentrations were higher in patients than in the control group (P = .018), no significant difference was determined between patient and control groups with respect to NSE concentrations (P = .801). A positive correlation was noted between levels of S100B and NSE (r = 0.388; P = .001). The S100B and NSE values were higher in unconscious patients than in the control group (P = .002 and P = .013, respectively). Furthermore, S100B and NSE values were higher in unconscious vs unconscious patients (P = .047 and P = .005, respectively).

Conclusion

Elevated serum S100B and NSE levels were associated with loss of consciousness in CO poisoning in this series of patients. Serum S100B and NSE may be useful markers in the assessment of clinical status in CO poisoning.     

The diagnostic value of neurogranin in patients with carbon monoxide poisoning: Can it show early neurological damage?

Background and aimCarbon monoxide poisoning is a toxicological emergency that causes neurological complications. High serum neurogranin can be detected in acute or chronic conditions where brain tissue is damaged. This study aimed to investigate the diagnostic value of serum neurogranin level and its role in demonstrating neurological damage in patients admitted to the emergency department with carbon monoxide poisoning.Materials and methodsThe study was conducted prospectively on patients with carbon monoxide poisoning (patient group) and healthy volunteers (control group). Demographic characteristics and serum neurogranin level of all participants and symptoms at admission, neurological examination findings, laboratory results, and Diffusion-Weighted Magnetic Resonance Imaging results of the patient group were recorded. We used an independent sample t-test to compare neurogranin levels and bivariate correlation analysis to compare the relationship between serum neurogranin levels and data belonging to the patient group.ResultsSixty eight participants (patient group, n = 36; control group, n = 32) were included in the study. Serum neurogranin level was significantly higher in patients with carbon monoxide poisoning (0.31 ± 0.16 ng/ml) compared to control group (0.22 ± 0.10 ng/ml) (p = 0.015). The mean Glasgow Coma Scale of the patients with carbon monoxide poisoning was 14.59 ± 0.23, and of Diffusion Weighted Magnetic Resonance Imaging results were completely normal in 94.4% (n = 34). There was no correlation between serum neurogranin level and Diffusion Weighted Magnetic Resonance Imaging results (r = −0.011; p = 0.953).ConclusionSerum neurogranin level may be a new diagnostic biomarker in patients admitted to the emergency department with carbon monoxide poisoning. The high serum neurogranin levels detected in patients with normal diffusion-weighted imaging after carbon monoxide poisoning suggest that there is neurological damage in these patients, even if imaging methods cannot detect it.     

Elevated S100B level in cerebrospinal fluid could predict poor outcome of carbon monoxide poisoning

Objective

S100B is a calcium-binding protein produced by astroglia in the brain and has been used as a marker of neuronal damage after brain trauma. We investigated the utility of S100B in cerebrospinal fluid (CSF) measured during the early phase of carbon monoxide (CO) poisoning in predicting the subsequent clinical course.

Methods

The study included 31 patients who were admitted to the hospital with loss of consciousness following CO poisoning. S100B levels were measured by enzyme-linked immunosorbent assay in CSF, and serum samples collected simultaneously within 24 hours and on the fourth day after CO exposure. All patients were followed for at least 3 months and divided into 3 groups based on the clinical course: persistent vegetative state (PVS), delayed encephalopathy (DE), and complete recovery with no complications (NC).

Results

During the 3-month period, 3 patients developed PVS, 5 developed DE, and 23 were classified as NC. The mean S100B levels in the CSF within 24 hours after CO exposure were higher in the PVS group (9.25 ng/mL) than in the DE (2.03 ng/mL) and NC groups (1.86 ng/mL). However, the mean serum S100B levels were not elevated in the 3 groups (0.21, 0.59, and 0.16 ng/mL, respectively).

Conclusion

Early elevation of S100B in CSF after CO poisoning could be a suitable predictor of subsequent development of PVS.     

Intoxication aiguë au monoxyde de carbone et séquelles neurologiques : de la physiologie à la clinique

Neuropsychiatric sequelae of carbon monoxide (CO) poisoning occur in up to 50% of all patients presenting with toxic CO levels. Neurological abnormalities include persistent (PNS) and delayed neurological sequelae (DNS) that occur after an asymptomatic period. Multiple hypotheses explain the mechanisms by which CO toxicity leads to cerebral injury including prolonged hypoxemia and dysfunction of intracellular mitochondrial cytochrome oxydase. Neurological examination shows impairments in memory and concentration as well as parkinsonism. Urinary and fecal incontinences represent common problems in severely CO-poisoned patients. No neuroprotective agents have yet demonstrated efficacy in preventing or improving delayed post-anoxic encephalopathy. Data on the effects of hyperbaric oxygen are conflicting because of the absence of any consensual protocol to treat CO poisonings.     

Epidemiology of Acute Carbon Monoxide Poisoning in a Spanish Region

Background: In Spain, as in most of the world, the incidence of acute carbon monoxide poisoning is probably underestimated. Methods: During an eighteen-month period we studied, by means of a standardized data collection form, all the cases of acute carbon monoxide poisoning that were diagnosed in 2 university hospitals. Results: During the study, 154 patients were diagnosed with carbon monoxide poisoning. The mean age was 32.2 ± 15.5 years. The two principal exposure sites were the kitchen (43%) and bathroom (23%). The majority of the cases related to malfunction of the water heater (30%) and of the central heating (23%) and 68% occurred in the home. Improper combustion of butane (31%), propane (13%), and natural gas (12%) were most frequent. The most prevalent clinical manifestations were headache (94%), dizziness (56%), nausea (45%), loss of consciousness (38%), and weakness (34%). Five patients died. In 14.4%, symptoms suggested delayed neurological syndrome. The largest number of cases of poisoning occurred during the months of December and January. Conclusions: Compared with previous Spanish series or with the antecedent year, acute carbon monoxide poisoning has a high prevalence in our region. Two factors appear to be essential to the accurate diagnosis of acute carbon monoxide poisoning: 1) the ability of emergency room physicians to recognize the clinical symptoms of carbon monoxide poisoning and 2) access to a carbon monoxide-oximeter.     

S100B protein in carbon monoxide poisoning: a pilot study

Carbon monoxide (CO) poisoning is the most common form of lethal poisoning. The aim of this prospective clinical study was to assess the possible role of S100B, the structural protein in the astroglia, as a biochemical marker of brain injury in carbon monoxide poisoning. Serum S100B determination was performed in 38 consecutive patients poisoned by carbon monoxide who were admitted to the Emergency Department (ED) in Ljubljana. All three unconscious patients had elevated S100B levels. The patient with the highest S100B died. S100B was elevated in two of the six patients with initial transitory unconsciousness at the scene. All 29 patients without loss of consciousness had normal S100B levels. Carbon monoxide poisoning appears to be associated with elevated S100B levels.     

Acute Carbon Monoxide Poisoning Risk of Late Sequelae and Treatment by Hyperbaric Oxygen

Abstract

The indications for hyperbaric oxygen therapy (HBO) in the treatment of acute carbon monoxide (CO) poisoning are discussed far too little in the literature. Depending on the author reasons for referral to a hyperbaric center include the carboxyhemoglobin level, change in state of consciousness or neurological abnormalities. In our opinion, HBO should be used on much wider indications than is usual, not only because of the rapid relief from symptoms it provides but mainly because it may prevent severe delayed sequelae. During a period of 9 months 230 patients with CO poisoning were admitted to our intensive care unit; 203 were treated with HBO and 27 with normobaric oxygen. Our indications for HBO treatment were: coma, pathological neurological findings or loss of consciousness during CO exposure irrespective of normal clinical findings on admission. Four patients died and the others were discharged 12 hours to 25 days after the incident. Seven patients had minor neurological problems within two weeks of discharge and which disappeared within one month. Two patients were re-hospitalized for neuropsychiatry sequelae and recovered in 3 and 6 months respectively. Neither the clinical status upon admission nor COHb predicted the outcome of the poisoning.

Referral to a HBO center should be considered when:

• the patient is comatose

• there are abnormal clinical findings

• patients have been unconsciousness during exposure, irrespective of whether they are conscious on admission and have normal clinical status.

     

The early elevation of interleukin 6 concentration in cerebrospinal fluid and delayed encephalopathy of carbon monoxide poisoning

Objective

This study was designed to investigate whether interleukin 6 (IL-6) in cerebrospinal fluid (CSF) in the early phase of carbon monoxide (CO) poisoning can be a predictive marker of delayed encephalopathy (DE).

Methods

Nine patients with CO poisoning were included in the study. Cerebrospinal fluid was sampled within 24 hours of the last exposure to CO, on hospital day 4, and once a week for at least 1 month to determine IL-6 and myelin basic protein concentrations. All patients were followed at least 3 months.

Results

Three patients demonstrated significant early IL-6 elevation in CSF, normal IL-6 level in CSF on day 4, and significant delayed myelin basic protein elevation in CSF. The 2 patients with the highest early IL-6 elevation in CSF developed DE. Interleukin 6 in serum was not related to DE.

Conclusion

Interleukin 6 in CSF at the early phase of CO poisoning may be a predictive marker of DE.     

Demographic characteristics and delayed neurological sequelae risk factors in carbon monoxide poisoning

AimCarbon monoxide (CO) is a colorless, odorless gas and tasteless. CO poisoning (COP) is one of the most frequently encountered inhalation poisonings. The most common cause of morbidity in COP is delayed neurological sequelae (DNS). DNS is the occurrence of neuropsychiatric findings within 2–240 days after discharge of patients with COP and there are no definitive diagnostic criteria.The aim of our study is; to determine the risk factors and incidence of DNS.MethodOur study is a retrospective, observational study. Patients with the diagnosis of COP in the emergency department between 2015 and 2016 were included in the study. Patients age, gender, findings in the initial physical examination (PE) and neurological examination (NE), blood carboxyhemoglobin (COHb) level, relation between hyperbaric oxygen (HBO) treatment and DNS were assessed.ResultsTotal of 72 patients were included in the study. Mean age was 33.43 ± 20.89. It was determined that pathological findings in the initial NE are a significant predictive factor for DNS (Odds ratio 18.600, p:0.004). Significant relation between NE and HBO treatment was present (p:00.1). There was no statistically significant relationship between initial COHb level and receiving HBO treatment (p:0.9). Median COHb level of patients with DNS was 30 (min:10, max: 43), median COHb level of patients without DNS was 25 (min:10, max:44) and there was no statistically significant relationship between the two groups according to COHb levels (p:0.7).ConclusionPathological findings in the initial neurological examination had a predictive value for delayed neurological sequelae in patients with carbon monoxide poisoning.     

三维斑点追踪成像评价急性一氧化碳中毒患者左心室收缩功能

目的 采用三维斑点追踪成像（3D-STI）技术评价急性一氧化碳中毒对左心室收缩功能的影响。方法 将109例急性一氧化碳中毒患者（研究组）分为轻（n=36）、中（n=40）及重度（n=33）亚组,于中毒后1 h、1周进行3D-STI检查,并检测碳氧血红蛋白（HbCO）和血清心肌肌钙蛋白I（cTnI）浓度;以105名健康志愿者为对照组。分析研究组与对照组各检测指标的差异及相关性。结果 急性一氧化碳中毒1 h,轻度亚组与对照组整体长轴应变（GLS）、整体面积应变（GAS）、整体圆周应变（GCS）、整体径向应变（GRS）及左心室射血分数（LVEF）差异无统计学意义（P均>0.05）,轻度亚组HbCO、cTnI均较对照组升高（P均<0.05）,中度亚组GLS、GAS较对照组降低（P均<0.05）,HbCO、cTnI较对照组升高（P均<0.05）;重度亚组GLS、GAS、GCS、GRS、LVEF较对照组降低（P均<0.05）,HbCO、cTnI较对照组升高（P均<0.05）。急性一氧化碳中毒后1周,轻、中度亚组与对照组GLS、GAS、GCS、GRS、LVEF、HbCO及cTnI差异无统计学意义（P均>0.05）;重度亚组GAS较对照组降低（P<0.05）,cTnI较对照组升高（P<0.05）。急性一氧化碳中毒1 h,研究组血清cTnI与GLS、GAS呈负相关（r=-0.626、-0.640,P均<0.05）。结论 3D-STI可早期诊断急性一氧化碳中毒引起的左心室收缩功能损害;GAS随血清cTnI含量升高而降低,是反映急性一氧化碳中毒左心室功能损害的较好指标。     

Therapeutic hyperbaric oxygen: help or hindrance in burn patients with carbon monoxide poisoning?

Although its efficacy is unproved, administration of hyperbaric oxygen (HBO) for the treatment of carbon monoxide poisoning is often carried out to prevent the development of acute and delayed neurologic sequelae. In burn patients with carbon monoxide poisoning the value of HBO also is unproved. This review of the clinical course of ten such patients showed major complications during the course of treatment: two patients suffered from eustachian tube occlusion, two patients had episodes of aspiration, one patient had seizure activity, and severe hypocalcemia developed in another. Progressive hypovolemia was seen in three patients; respiratory acidosis was evident in four. There were three episodes of cardiac dysrhythmia. Seven of the ten patients survived. The authors state that the efficacy of HBO in carbon monoxide poisoning must be studied further. Based on their experience and a review of the literature, they contend that important delayed neurologic sequelae are rare, and further, that they occur and resolve with or without HBO. Multicenter randomized clinical trials with controlled follow-up are needed to assess the actual incidence of neuropsychiatric sequelae and to evaluate the efficacy of HBO.     

粤东地区住院患者一氧化碳急性中毒原因分析及治疗护理对策

目的：探讨粤东地区住院患者急性一氧化碳（CO）急性中毒的原因，并针对不同中毒程度采用不同的处理措施。方法对本院急性CO中毒住院治疗的患者319例进行回顾性分析。结果本地区CO中毒人群大部分为年龄≤19岁及年龄≥60岁患者；急性中毒原因主要是煤气管道泄漏、热水器使用不当等；中毒程度以轻、中度为主；辅助检查血COHb均为阳性，多伴有外周血象白细胞及中性粒细胞计数增高。结论青少年和老年人是粤东地区CO中毒的主要人群，及时救治是预防CO中毒后遗症的关键。     

急性一氧化碳中毒患者血浆同型半胱氨酸浓度与血清TNF—α水平的相关性临床研究

目的探讨急性一氧化碳（CO）中毒患者血浆同型半胱氨酸（Hcy）浓度与血清肿瘤坏死因子-α（TNF-α）水平与病情严重程度和对预后的关系。方法将82例急性CO中毒患者分为三组：A组轻度组、B组中度组和C组重度组,应用ELISA法对82例急性CO中毒患者的血浆Hcy浓度与血清TNF-α水平进行检测。结果重度组与中度组Hcy与TNF-α水平均明显高于轻度中毒组（P〈0．01）,且重度组明显高于中度组（P〈0．05）;迟发性脑病患者均发生在重度组,其Hey与TNF-α水平与其他组的比较差异有显著性（P〈0．05）。结论检测急性CO中毒患者的血浆Hcy浓度与血清TNF-α水平,有助于评估急性期脑组织受损的严重程度及预测迟发性脑病的发生。     

Carbon monoxide poisoning: correlation of neurological findings between accident and emergency departments and a hyperbaric unit

Objectives—To investigate and quantify the differences in neurological examination findings in patients acutely poisoned with carbon monoxide, between initial assessment at accident and emergency (A&E) departments and subsequently at a hyperbaric unit.

Methods—Retrospective case note review of all patients referred to the Hull Hyperbaric Unit for treatment of acute carbon monoxide poisoning between August 1998 and August 1999. Patients who were ventilated or less than 16 years old were excluded because of difficulty in assessing their neurological status.

Results—Thirty patients were included for analysis. The mean duration from exposure to assessment in A&E was four hours while patients were reviewed on average three hours later at the hyperbaric unit. Referrals came from 14 different hospitals. A history of loss of consciousness accounted for 70% of referrals. A mean of 3.2 neurological signs per patient was documented in A&E compared with 9.2 at the hyperbaric unit. Seventy nine per cent of abnormal neurological signs were not detected at A&E departments compared with 3% at the hyperbaric unit. The major source of discrepancy was in sharpened Rhomberg's test and heel-toe gait, in 13% of patients examined in A&E departments these signs were recorded as abnormal compared with 90% at the hyperbaric unit.

Conclusion—There is a large discrepancy in neurological findings between assessment in A&E departments and the Hull Hyperbaric Unit. A number of factors may account for this including interobserver variation, patient deterioration during transfer, poor documentation, lack of understanding of the sequelae of carbon monoxide poisoning and inadequate examinations. Further research is required to quantify the impact of the various factors that may contribute to the differences in neurological findings.

     

Effects of intravascular laser phototherapy on delayed neurological sequelae after carbon monoxide intoxication as evaluated by brain perfusion imaging: A case report and review of the literature

BACKGROUNDDelayed neurological sequelae (DNS) caused by carbon monoxide (CO) intoxication poses considerable treatment challenges for clinical practitioners. In this report, we used nuclear medicine imaging and the Mini-Mental State Examination (MMSE) to evaluate the effectiveness of intravascular laser irradiation of blood (ILIB) therapy for the management of DNS.CASE SUMMARYA 51-year-old woman presented to our medical center experiencing progressive bradykinesia, rigidity of limbs, gait disturbance, and cognitive impairment. Based on her neurological deficits, laboratory tests and imaging findings, the patient was diagnosed with delayed neurological sequelae of CO intoxication. She received intensive rehabilitation and ILIB therapy during 30 sessions over 2 mo after diagnosis. Brain single-photon emission computed tomography was performed both prior to and after ILIB therapy. The original hypoperfusion area in bilateral striata, bilateral frontal lobe, right parietal lobe, and bilateral cerebellum showed considerable improvement after completion of therapy. The patient’s MMSE score also increased markedly from 6/30 to 25/30. Symptoms of DNS became barely detectable, and the woman was able to carry out her daily living activities independently.CONCLUSIONILIB therapy could facilitate recovery from delayed neurological sequelae in patients with CO intoxication, as demonstrated by improved cerebral blood flow and functional outcomes in our patient.     

Serum S100 protein could predict altered consciousness in glyphosate or glufosinate poisoning patients

Background: Central nervous system (CNS) complications such as seizures and reduced consciousness are important in glufosinate and may occur in severe glyphosate poisoning. The aim of this study was to assess the possible role of serum S100B protein as a biochemical marker of CNS complications associated with glyphosate or glufosinate poisoning.

Methods: The study enrolled 40 patients (23 glyphosate poisoning and 17 glufosinate poisoning). Altered consciousness and seizure were observed during hospitalization. S100B level was measured with fully automated modular analytic E170 system using electrochemoluminometric immunoassay.

Results: Among 40 patients, neurologic features were observed in 12 patients with a median time to onset of 21.5 (IQR 8.25–24.75) h. Serum S100B concentrations measured on admission were higher in the group with neurologic features than in the group without neurologic features [0.148?μg/L (IQR 0.128–0.248) vs. 0.072?μg/L (IQR 0.047–0.084), p?Conclusions: In our pilot study, S100B was a significant predictor of neurologic complications in patients with glyphosate and glufosinate poisoning. Large prospective cohorts are needed to confirm this finding.