A protocol for a pilot study to assess the feasibility of a randomised clinical trial of perioperative intravenous lidocaine on colorectal cancer outcome after surgery (FLICOR trial).

Background: Cancer recurrence after curative cancer surgery significantly impacts patients and healthcare services. Before surgery, a small number of clinically undetectable circulating tumour cells are often present. The surgical stress response promotes the distribution and proliferation of circulating tumour cells leading to cancer recurrence and metastasis. Preclinical evidence suggests that lidocaine may exert 'anti-cancer' effects and alleviate pro-metastatic environments. The Feasibility Study of Lidocaine Infusion During Bowel Cancer Surgery for Cancer Outcome (FLICOR) will assess the feasibility of conducting a clinical trial on perioperative intravenous lidocaine infusion for postoperative colorectal cancer outcomes. Methods: The study is a double-blinded, randomised, controlled pilot study for a full trial comparing intravenous lidocaine administration at 1.5 mg kg-1 bolus followed by 1.5 mg kg-1 h-1 infusion for 24 h with placebo in patients undergoing minimally invasive (laparoscopy or robotic) colorectal cancer surgery. The feasibility of data collection instruments will be measured, including those for future economic evaluation and clinical and patient-reported outcomes. For the exploratory outcomes, blood samples will be collected before and after surgery on days 0, 1, and 3. Recruitment is planned for two NHS Trusts over 6 months with a 12-month follow-up. Patients and clinicians will be asked for their feedback on the study process. Dissemination plan: Study data will be disseminated to trial participants, the public, and academic communities. The work will be presented at national and international conferences to stimulate interest and enthusiasm for centres to participate in the future definitive trial. This research will also be published in peer-reviewed open-access journals. Clinical trial registration: ISRCTN29594895 (ISRCTN), NCT05250791 (ClinicalTrials.gov). Protocol version number and date: 3.0, February 8, 2023.

Iatrogenic subglottic tracheal stenosis after tracheostomy and endotracheal intubation: A cohort observational study of more severity in keloid phenotype.

BACKGROUND: Tracheostomy and endotracheal intubation can result in subglottic tracheal stenosis, and predisposition to keloid scar formation can increase stenosis risk after tracheal injury. This study aims to compare the incidence and severity of subglottic tracheal stenosis in keloid and non-keloid patients following iatrogenic tracheal injury, in particular tracheostomy. METHODS: From 2012 to 2017, 218 573 patients were intubated for surgery; 2276 patients received tracheostomy in People's Hospital of Zhengzhou University, China. Among these patients, 133 patients, who developed tracheal stenosis after intubation and/or tracheostomy, were divided into keloid or non-keloid groups; their Myer and Cotton grading of tracheal stenosis, time-to-onset of airway stenosis, and treatment outcome were assessed and compared. RESULTS: The percentages of high grade (Myer and Cotton grading III/IV) tracheal stenosis were higher among keloid patients than non-keloid patients (intubation: 83.3% vs 25.7%; tracheostomy: 77.7% vs 33.3%). Time-to-onset of airway stenosis following intubation (tracheostomy) was 27 ± 5 (38 ± 13) and 41 ± 7 (82 ± 14) days for keloid and non-keloid patients, respectively (P < 0.01). The incidence of tracheal stenosis is higher in keloid than non-keloid subjects (19.4% vs 1.82%, P < 0.001). Keloid patients also required more frequent treatment (P < 0.01) of longer duration, yet cure rate was significantly lower (P < 0.01). CONCLUSIONS: Our study suggests that tracheostomized patients with keloid phenotype are more susceptibility to develop iatrogenic tracheal stenosis of greater severity and with poorer treatment outcome. Greater cautions may be required when performing tracheostomy in keloid subjects. More substantive analysis is warranted to establish keloid phenotype as a risk factor for tracheal stenosis.