Post-operative pain management in head and neck cancer patients: predictive factors and efficacy of therapy.

There is increasing interest about all aspects of pain sensation for patients undergoing head and neck surgery, and efforts have been made to better assess, monitor and reduce the occurrence of pain. The aetiology of pain is considered to be "multifactorial", as it is defined by several features such as personal experience, quality perception, location, intensity and emotional impact. The aim of this paper is: (i) to evaluate the efficacy of analgesic treatment in patients with head and neck cancer treated by surgery, and (ii) to study the variables and predictive factors that can influence the occurrence of pain. A total of 164 patients, affected by head and neck cancer and surgically treated, between December 2009 and December 2013, were included in this study. Data collected include age, gender, assessment of anaesthetic risk, tumour localisation, pathological cancer stage, TNM stage, type of surgery performed, complexity and duration of surgery, post-operative complications, postoperative days of hospital stay and pain evaluation on days 0, 1, 3 and 5 post-surgery. We studied the appropriateness of analgesic therapy in terms of incidence and prevalence of post-operative pain; we also related pain to patient characteristics, disease and surgical treatment to determine possible predictive factors. The population studied received adequate pain control through analgesic therapy immediately post-surgery and in the following days. No associations between gender, age and post-operative pain were found, whereas pathological cancer stage, complexity of surgery and tumour site were significantly associated with the risk of post-operative pain. Adequate pain control is essential in oncological patients, and particularly in head and neck cancer patients as the prevalence of pain in this localisation is reported to be higher than in other anatomical sites. Improved comprehension of the biological and psychological factors that characterise pain perception will help to enhance its control in the future.

Fractalkine protein localization and gene expression in mouse brain.

Few chemokines are expressed constitutively in the brain at detectable levels; amongst them is fractalkine. We analyzed the distribution of fractalkine in the mouse brain with the aim of giving a neuroanatomical support to the study of its physiological function. To this end, we carried out an analysis of fractalkine protein localization and gene expression. An anti-fractalkine antibody was produced and used to perform an immunohistochemical study. The results indicated a high level of fractalkine protein in cortex, hippocampus, basal ganglia, and olfactory bulb. In particular, the presence of abundant immunoreactive neurons was observed in layers II, III, V, and VI of the cortex. In the hippocampus, the CA1 region was the most intensely labeled, but immunoreactive neurons were present also in CA2 and CA3, whereas in the basal ganglia, immunoreactive cells were observed in the caudate putamen. Other brain structures such as the brainstem showed a few scattered immunoreactive cells. The presence of fractalkine immunoreactive fibers was revealed only in the olfactory bulb and in the anterior olfactory nuclei. Gene expression study results, obtained by both semiquantitative PCR and in situ hybridization, matched protein localization with the highest levels of fractalkine transcript detected in the hippocampus, cortex, and striatum. The present study showed that fractalkine protein and mRNA are constitutively expressed at a high level in forebrain structure, but are almost absent in the hindbrain. Furthermore, localization at the cellular body level would suggest a paracrine or cell-to-cell interaction role for fractalkine more than a neurotransmission modulatory function.

Validation of severity scoring systems SAPS II and APACHE II in a single-center population.

OBJECTIVE: To validate two severity scoring systems, the Simplified Acute Physiology Score (SAPS II) and Acute Physiology and Chronic Health Evaluation (APACHE II), in a single-center ICU population. DESIGN AND SETTING: Prospective data collection in a two four-bed multidisciplinary ICUs of a teaching hospital. PATIENTS AND METHODS: Data were collected in ICU over 4 years on 1,721 consecutively admitted patients (aged 18 years or older, no transferrals, ICU stay at least 24 h) regarding SAPS II, APACHE II, predicted hospital mortality, and survival upon hospital discharge. RESULTS: At the predicted risk of 0.5, sensitivity was 39.4 % for SAPS II and 31.6 % for APACHE II, specificity 95.6 % and 97.2 %, and correct classification rate 85.6 % and 85.5 %, respectively. The area under the ROC curve was higher than 0.8 for both models. The goodness-of-fit statistic showed no significant difference between observed and predicted hospital mortality (H = 7.62 for SAPS II, H = 3.87 for APACHE II; and C = 9.32 and C = 5.05, respectively). Observed hospital mortality of patients with risk of death higher than 60 % was overpredicted by SAPS II and underpredicted by APACHE II. The observed hospital mortality was significantly higher than that predicted by the models in medical patients and in those admitted from the ward. CONCLUSIONS: This study validates both SAPS II and APACHE II scores in an ICU population comprised mainly of surgical patients. The type of ICU admission and the location in the hospital before ICU admission influence the predictive ability of the models.

Respiratory effects of pharingeal gas insufflation in patients with chronic obstructive pulmonary disease.

OBJECTIVE: To evaluate the effects of pharyngeal gas insufflation (PGI) in clinically stable patients with chronic obstructive pulmonary disease (COPD). DESIGN: Prospective study in humans. SETTING: Department of Intensive Care Medicine at a University Hospital. PATIENTS: Seven clinically stable COPD patients. INTERVENTION: Pharyngeal dry fresh air insufflation (PGI) with a continuous flow rate of 4 L/min was given via a nasal catheter placed into the oropharynx. Baseline measurements with zero flow were made at the beginning and end of the test. After an equilibration period of 1 h at each stage, arterial blood samples were analyzed every 5 min until PaCO2 variation less than 5% confirmed the achievement of a steady state. Thereafter expiratory flow signal and expiratory gas were collected over a period of 3 min and arterial blood was sampled after 1'30" and 2'30" from the beginning of the test for the measurement of effective expiratory volume (VE eff), respiratory rate (RR), tidal volume (VT), dead space fraction (VD/VT), dead space (VD), alveolar ventilation (VA), total expiratory time (TE min), and PaCO2, respectively. RESULTS: During PGI VT, VD/VT, VD and VE eff fell significantly from baseline values, RR was slightly reduced and VA, TE min and PaCO2 remained unchanged throughout the study. CONCLUSIONS: Although in our study the effect of PGI on VD could be overestimated since our device for expiratory gas flow measurement and collection significantly enlarged the anatomical dead space receiving the washout effect of the fresh gas insufflation, under the experimental conditions PGI produces a reduction in VD and VD/VT, and, as a consequence, a significative reduction in respiratory requirements in clinically stable COPD patients. If confirmed in clinical settings, potential advantages of PGI could include: a) reduction of the work of breathing in patients with intact neuro-respiratory coupling; b) minimizing hypercapnic side effects of oxygen therapy often seen in COPD patients.

Additional inspiratory resistance imposed by the laryngeal mask airway: in vitro versus in vivo comparison.

The present study was designed: (a) to compare the additional inspiratory laryngeal mask airway (LMA) resistance measured in vitro during simulated ventilation and in vivo in five anaesthetised and mechanically ventilated patients; and (b) to evaluate the resistive pressure drop along the length of the LMA. After the differential pressure across the mask was measured, the pressure-flow relationship was characterised by Rohrer's equation and in vitro and in vivo resistance was calculated. Thereafter, the distal pressure measuring point was moved along the length of the LMA and differential pressure was measured at each point under in vitro and in vivo conditions. Values for resistance were approximately twice as great in vivo as those obtained in vitro, with most of the resistive pressure drop occurring across the vertical bars, especially when measured in vivo. We conclude that in vivo positioning of the LMA significantly increases resistance because of the configurational changes occurring when the LMA is in situ.