The volume and pH of residual pharyngeal fluid aspirated from the TaperGuard Evac™ Endotracheal Tube following elective surgery: a prospective pilot study.

BACKGROUND: Oropharyngeal suctioning prior to extubation aims to minimize postextubation tracheal soiling from remaining fluid. We investigated the amount and nature of any fluid remaining after such suctioning and contributing factors. METHODS: ASA I - III patients undergoing elective surgery under general anesthesia with endotracheal intubation participated in this prospective observational pilot study. Following oropharyngeal suctioning immediately prior to extubation, a dedicated port of the endotracheal tube (TaperGuard Evac™ Endotracheal Tube) was aspirated. The amount and pH of residual fluid was recorded. Data collection included age, sex, body mass index, comorbidities, ASA status, procedure type and duration. The Chi-Square, Wilcoxon Rank-Sum, t-tests, and univariate regression analysis were used as appropriate. RESULTS: Ninety-eight patients completed the study. The mean aspirated volume in 38 (38.8%) patients was 0.9 ± 1.3 mL and sixty patients (61.2%) had no aspirate. A body mass index of ≥ 30 kg/m2 was associated with the presence of fluid (P=0.03), and a higher volume (P=0.03). The fluid pH was 7 ± 0.81 (mean ± SD). A duration of surgery ≥ 120 minutes predicted a lower pH. CONCLUSION: The prevalence and amount of residual fluid after oropharyngeal suctioning was low and likely clinically insignificant. A higher body mass index was associated with a higher incidence and volume of residual fluid. Longer procedure duration determined a slightly lower pH, with a mildly acidic pH range. The possibility of a lower fluid pH after prolonged surgery contributing to postoperative sore throat via mucosal irritation warrants investigation.

Pain catastrophizing and neural responses to pain among persons with fibromyalgia.

Pain catastrophizing, or characterizations of pain as awful, horrible and unbearable, is increasingly being recognized as an important factor in the experience of pain. The purpose of this investigation was to examine the association between catastrophizing, as measured by the Coping Strategies Questionnaire Catastrophizing Subscale, and brain responses to blunt pressure assessed by functional MRI among 29 subjects with fibromyalgia. Since catastrophizing has been suggested to augment pain perception through enhanced attention to painful stimuli, and heightened emotional responses to pain, we hypothesized that catastrophizing would be positively associated with activation in structures believed to be involved in these aspects of pain processing. As catastrophizing is also strongly associated with depression, the influence of depressive symptomatology was statistically removed. Residual scores of catastrophizing controlling for depressive symptomatology were significantly associated with increased activity in the ipsilateral claustrum (r = 0.51, P < 0.05), cerebellum (r = 0.43, P < 0.05), dorsolateral prefrontal cortex (r = 0.47, P < 0.05), and parietal cortex (r = 0.41, P < 0.05), and in the contralateral dorsal anterior cingulate gyrus (ACC; r = 0.43, P < 0.05), dorsolateral prefrontal cortex (r = 0.41, P < 0.05), medial frontal cortex (r = 0.40, P < 0.05) and lentiform nuclei (r = 0.40, P < 0.05). Analysis of subjects classified as high or low catastrophizers, based on a median split of residual catastrophizing scores, showed that both groups displayed significant increases in ipsilateral secondary somatosensory cortex (SII), although the magnitude of activation was twice as large among high catastrophizers. Both groups also had significant activations in contralateral insula, SII, primary somatosensory cortex (SI), inferior parietal lobule and thalamus. High catastrophizers displayed unique activation in the contralateral anterior ACC, and the contralateral and ipsilateral lentiform. Both groups also displayed significant ipsilateral activation in SI, anterior and posterior cerebellum, posterior cingulate gyrus, and superior and inferior frontal gyrus. These findings suggest that pain catastrophizing, independent of the influence of depression, is significantly associated with increased activity in brain areas related to anticipation of pain (medial frontal cortex, cerebellum), attention to pain (dorsal ACC, dorsolateral prefrontal cortex), emotional aspects of pain (claustrum, closely connected to amygdala) and motor control. These results support the hypothesis that catastrophizing influences pain perception through altering attention and anticipation, and heightening emotional responses to pain. Activation associated with catastrophizing in motor areas of the brain may reflect expressive responses to pain that are associated with greater pain catastrophizing.