Effect of different degrees of adenoid hypertrophy on pediatric upper airway aerodynamics: a computational fluid dynamics study.

To improve the diagnostic accuracy of adenoid hypertrophy (AH) in children and prevent further complications in time, it is important to study and quantify the effects of different degrees of AH on pediatric upper airway (UA) aerodynamics. In this study, based on computed tomography (CT) scans of a child with AH, UA models with different degrees of obstruction (adenoidal-nasopharyngeal (AN) ratio of 0.9, 0.8, 0.7, and 0.6) and no obstruction (AN ratio of 0.5) were constructed through virtual surgery to quantitatively analyze the aerodynamic characteristics of UA with different degrees of obstruction in terms of the peak velocity, pressure drop (△P), and maximum wall shear stress (WSS). We found that two obvious whirlpools are formed in the anterior upper part of the pediatric nasal cavity and in the oropharynx, which is caused by the sudden increase in the nasal cross-section area, resulting in local flow separation and counterflow. In addition, when the AN ratio was ≥ 0.7, the airflow velocity peaked at the protruding area in the nasopharynx, with an increase 1.1-2.7 times greater than that in the nasal valve area; the △P in the nasopharynx was significantly increased, with an increase 1.1-6.8 times greater than that in the nasal cavity; and the maximum WSS of the posterior wall of the nasopharynx was 1.1-4.4 times larger than that of the nasal cavity. The results showed that the size of the adenoid plays an important role in the patency of the pediatric UA.

Involvement of spinal cannabinoid receptor type 2 in the analgesia effect of hyperbaric oxygen treatment on paclitaxel-induced neuropathic pain.

BACKGROUND: Chemotherapy-induced neuropathic pain (CINP) is intractable, and spinal cannabinoid receptors (CBRs) are potential therapeutic targets for CINP. Previous studies demonstrated that hyperbaric oxygen (HBO2) may contribute in alleviating specific peripheral neuropathic pain. However, neither CINP nor CBR have been clarified. We hypothesized that HBO2 is capable of alleviating CINP, and the effect could be explained by the activation of spinal CBRs. METHODS: A series of paclitaxel-induced CINP models were established on male Sprague-Dawley rats. Then HBO2 treatment was administered for seven consecutive days at 2.5 atmospheres absolute. Two groups were treated with AM251 (an antagonist of CBR type-1, CBR1) or AM630 (an antagonist of CBR type-2, CBR2) respectively 30 minutes before each HBO2 treatment. The mechanical withdrawal threshold was assessed before, during and at two weeks after HBO2 treatment. Lumbar spinal cords were collected for Western blot analysis of CBR1, CBR2, GFAP and CD11b, and ELISA analysis of proinflammatory cytokines IL-1ß and TNF-α. RESULTS: A mechanical allodynia was successfully exhibited and the spinal GFAP, CD11b, IL-1ß and TNF-α significantly increased after the modeling, and these effects could be further reversed by HBO2 treatment, which could be blocked by AM630, other than AM251. CONCLUSION: HBO2 treatment can alleviate paclitaxel-induced neuropathic pain, and be mediated by CBR2. Spinal glial cells and proinflammatory cytokines are involved in this process.

[The value of bispectral index in the unconscious patients with acute brain injury due to different pathogenic factors].

OBJECTIVE: To observe the differences in bispectral index (BIS) in unconscious patients with acute brain injury due to different pathogenic factors, and approach its clinical significance. METHODS: A retrospective study was conducted. One hundred and twenty-two unconscious patients with acute brain injured admitted to the intensive care unit (ICU) from March 2009 to August 2012 were involved. According to the pathogenic factors, all patients were divided into direct injury group (n=66) and indirect injury group (n=56). Based on BIS value, all patients were divided into the BIS<60 group (n=80) and the BIS≥60 group (n=42). The BIS was continuously measured for 12 hours during the first 3 days, or 24 hours after stoppage of sedative after admission to ICU. The mean value of BIS (BISmean) was evaluated. The acute physiology and chronic health evaluationII (APACHEII) score, probability of survival (PS) and Glasgow coma score (GCS) were recorded. On the same day, the serum protein S100 and neuron-specific enolase (NSE) were determined. The mortality and the rate of the poor neurological outcome were analyzed. RESULTS: (1) There were no significant differences in the age, sex, APACHEII score, PS and days of stay in ICU between the direct and indirect injury groups. (2) BISmean and GCS in direct injury group were significantly lower than those of the indirect injury group [BISmean: 39.0 (2.5, 58.0) vs. 59.0 (42.0, 71.0), GCS score: 3 (3, 5) vs. 4 (3, 6), both P<0.01], while serum S100 levels was significantly higher [2.30 (0.75, 6.66) mg/L vs. 0.84 (0.40, 3.62) mg/L, P<0.01]. There was no significant difference in the NSE level between the direct and indirect injury groups. (3) The mortality rate and poor neurological outcome rate in BIS<60 group were significantly higher than the BIS≥60 group (mortality rate: 67.50% vs. 40.48%, poor neurological outcome rate: 86.25% vs. 66.67%, P<0.01 and P<0.05). In the BIS<60 group, there were no significant differences in the mortality and poor neurological outcome rate between direct and indirect injury group. CONCLUSIONS: There are differences in pathogenic factors, the injury mechanism, and the degree of the brain injury between the direct and indirect injury groups. BIS monitoring could help judge the degree of different kinds of brain injury. BIS<60 indicates poor prognosis and neurological outcome in spite of the inducing factor of brain injury.

[Evaluation of continuous monitoring of bispectral index in prognosis in patients with acute brain injury].

OBJECTIVE: To discuss the effect of continuous monitoring of bispectral index (BIS) on the prognosis of patients with acute brain injury. METHODS: A retrospective study was carried out, 61 patients with acute brain injury admitted to the intensive care unit (ICU) from March 2009 to July 2010 were divided into survival group (n=25) and death group (n=36). The BIS was continuously monitored for 12 hours within the first 3 days or 24 hours after stoppage of sedative after admission to ICU. The mean value of BIS (BISmean), the maximal value of BIS (BISmax), and the minimal value of BIS (BISmin) were evaluated. At the same time, the acute physiology and chronic health evaluationII (APACHEII) score, probability of survival (PS) and Glasgow coma score (GCS) were evaluated. The values of serum S100 protein and neuron-specific enolase (NSE) were determined. The relationship between BISmean and GCS, S100 protein and NSE were respectively analyzed. RESULTS: (1)There was no significant difference in the sex, age, or duration of mechanical ventilation between two groups. APACHEII score in death group was significantly higher than the survival group (27.36±5.99 vs. 23.28±6.69), PS was significantly lower than the survival group (0.31±0.17 vs. 0.49±0.19), and length of stay in ICU (days) was significantly lower than that of the survival group (6.33±4.48 vs. 27.88±54.46), P<0.05 or P<0.01. (2) BISmean, BISmax, BISmin, GCS in death group were significantly lower than those in the survival group (BISmean: 35.45±28.31 vs. 55.91±17.53, BISmax: 51.92±34.24 vs. 74.84±16.58, BISmin: 22.39±24.83 vs. 39.68±15.72, GCS score: 3.64±1.19 vs. 5.60±2.22), P<0.05 or P<0.01, while serum S100 protein and NSE levels were significantly higher than the survival group [S100 protein (µg/L): 7.54±10.49 vs. 1.18±1.57, NSE (µg/L): 120.74±109.01 vs. 49.83±54.94], both P<0.01. (3) By bivariate analysis, BISmean was positively correlated with GCS (r=0.379, P=0.003), whereas it was found to be negatively correlated with S100 protein and NSE levels (r1=-0.418, P1=0.001; r2=-0.290, P2=0.023). CONCLUSION: BIS monitoring can be applied as an early objective indicator to evaluate the prognosis of the acute brain injured patients with the characteristics of being noninvasive, intuitive, easy-to-manipulate, and non-stop monitoring.

[Role of neuron specific enolase and S100 protein in evaluation of brain damage in patients resuscitated from cardiac arrest].

OBJECTIVE: To investigate the prognostic value of serum neuron specific enolase (NSE) and S100 protein in evaluation of brain damage in patients resuscitated from cardiac arrest (CA). METHODS: According to whether the patients regained consciousness after 6 months or not, 25 patients after cardiopulmonary resuscitation (CPR) were divided into 2 groups, and blood samples were obtained for determination of NSE and S100 protein at 2, 12, 24, 48 and 72 hours after recovery of spontaneous circulation (ROSC), then the values at each time point were compared between 2 groups and also with that of 7 healthy volunteers. Receiver operator characteristic (ROC) curves of serum NSE and S100 protein were depicted and used area under curve (AUS) to scale the ability in evaluating the state of consciousness in patients after CPR. RESULTS: (1)The levels of serum NSE at 12, 48 and 72 hours and S100 protein at 2, 12, 48 and 72 hours were significantly higher in patients who did not regain consciousness compared with patients who regained consciousness (all P<0.01). (2)Compared with healthy volunteers, the levels of NSE at 12 and 24 hours and S100 protein at 12 hours were higher in patients who regained consciousness (all P<0.05), the levels of NSE at all time points and S100 protein at 12, 48 and 72 hours were significantly higher in patients who did not regain consciousness (P<0.05 or P<0.01). (3)Area under curve AUC(NSE) =0.848 (P=0.000), AUC(S100) =0.896 (P=0.000), therefore both serum NSE and S100 protein had diagnostic value for predicting whether patients resuscitated from CA could regain consciousness or not. Serum S100 protein cut-off was 0.165 microg/L, with a sensitivity of 94.4%, a specificity of 100%, a positive predictive value of 100%, a negative predictive value of 80% and an accuracy of 95.5% at 2 hours after ROSC. Serum NSE cut-off was 45.6 microg/L, all values reached 100% 48 hours after ROSC. CONCLUSION: Measurement of serum NSE and S100 protein concentrations can help judge the degree of brain damage and whether patients can regain consciousness after CPR. It will be more valuable to prognosticate a serious and continuous brain damage with dynamic observation of the serum NSE together with S100 protein.