Awake nasotracheal intubation with a 300-mm working length fiberscope: a prospective observational feasibility trial

Background: Awake fiberoptic tracheal intubation is an established method of securing difficult airways, but there are some reservations about its use because many practitioners find it technically complicated, time-consuming, and unpleasant for patients. Our main goal was to test the safety and efficacy of a 300-mm working length fiberscope (video rhino-laryngoscope) when used for awake nasotracheal intubation in difficult airway cases. Methods: This was a prospective, single-center study involving adult patients, having an ASA physical status between I and IV, with laryngopharyngeal pathology causing distorted airway anatomy. Awake nasotracheal intubation, using topical anesthesia and light sedation, was performed using a 300 mm long and 2.9 mm diameter fiberscope equipped with a lubricated reinforced endotracheal tube. The primary outcomes were the success and duration of the procedure. Patients’ periprocedural satisfaction and other incidents were recorded. Results: We successfully intubated all 25 patients included in this study. The mean ±SD duration of the procedure, starting from the passage of the intubating tube through one of the nostrils until the endotracheal intubation, was 76 ± 36 seconds. Most of the patients showed no discomfort during the procedure with statistical significance between the No reaction Group with the Slight grimacing Group (95%CI 0.13, 0.53, p = 0.047) and the Heavy grimacing Group (95%CI 0.05, 0.83, p = 0.003). The mean ±SD satisfaction score 24 hours post-intervention was 1.8 ± 0.86 – mild discomfort. No significant incidents occurred. Conclusions: Our study showed that a 300-mm working length flexible endoscope is fast, safe, and well-tolerated for nasotracheal awake intubation under challenging airways

Paradoxical Effect of Grape Pomace Extract on Cisplatin-Induced Acute Kidney Injury in Rats

Cisplatin is one of the most used drugs in the therapy of different types of cancer. However, its use is limited by nephrotoxicity. This study investigated the effects of a commercially available grape pomace extract (GE) from Vitis vinifera on cisplatin-induced kidney toxicity in rats. Sixty-four male Wistar albino rats were randomly divided into eight groups. Groups 1–3 were controls, receiving 0.9% saline and doses 1 and 2 of GE respectively. Cisplatin was given to groups 4–8. Two groups received pretreatment with GE, while another two groups received pre- and post-treatment with GE. Blood samples were collected and all animals sacrificed. Kidneys were harvested for histopathological analysis. GE significantly increased blood creatinine and urea levels, the severity of kidney histopathological damage, and mortality in all cisplatin groups, except for group 7 which received pre- and post-treatment with a low dose of GE. Renal toxicity was determined by mortality and severe histopathological renal lesions. Additionally, the serum total antioxidant capacity (TAC) was not significantly modified in the treated groups compared to the control. These results indicate that the GE did not have a protective effect on cisplatin-induced nephrotoxicity; on the contrary, GE accentuated the toxic effect of cisplatin.</jats:p

Paradoxical Effect of Grape Pomace Extract on Cisplatin-Induced Acute Kidney Injury in Rats

Cisplatin is one of the most used drugs in the therapy of different types of cancer. However, its use is limited by nephrotoxicity. This study investigated the effects of a commercially available grape pomace extract (GE) from Vitis vinifera on cisplatin-induced kidney toxicity in rats. Sixty-four male Wistar albino rats were randomly divided into eight groups. Groups 1&ndash;3 were controls, receiving 0.9% saline and doses 1 and 2 of GE respectively. Cisplatin was given to groups 4&ndash;8. Two groups received pretreatment with GE, while another two groups received pre- and post-treatment with GE. Blood samples were collected and all animals sacrificed. Kidneys were harvested for histopathological analysis. GE significantly increased blood creatinine and urea levels, the severity of kidney histopathological damage, and mortality in all cisplatin groups, except for group 7 which received pre- and post-treatment with a low dose of GE. Renal toxicity was determined by mortality and severe histopathological renal lesions. Additionally, the serum total antioxidant capacity (TAC) was not significantly modified in the treated groups compared to the control. These results indicate that the GE did not have a protective effect on cisplatin-induced nephrotoxicity; on the contrary, GE accentuated the toxic effect of cisplatin