We present case report of 62-year-old man who underwent total laryngectomy, bilateral neck dissection and radiotherapy due to laryngeal cancer. After 11 months he was reoperated because of a local recurrence. The second procedure was complicated with postoperative wound dehiscence in tracheostomy site which was successfully treated with negative pressure wound therapy. We indicate the difficulties and point technical solutions for negative pressure dressing around the airway.

Purpose Adequate tissue oxygenation is essential for effective skin wound healing. Hypoxia contributes to impaired healing and chronic wound formation. Obstructive sleep apnea (OSA) affects nearly one billion adults worldwide, and up to 80% of cases remain undiagnosed. OSA causes intermittent hypoxia (IH), with repetitive cycles of oxygen desaturation and reoxygenation during sleep. The molecular pathways activated by IH differ from those induced by acute and chronic hypoxia. We propose that OSA may contribute to impaired wound healing in two ways. Indirectly, by promoting comorbidities such as diabetes, hypertension, and obesity. Directly, through IH and its effects at the cellular and tissue level. Methods PubMed/MEDLINE, Scopus, and Web of Science were searched through August 2026 for preclinical and clinical studies on OSA, IH, and wound healing. Results To our knowledge, this is the first review to integrate cellular mechanisms, preclinical evidence, and clinical data on this topic. We describe the IH-driven mechanisms that may contribute to impaired wound healing, including reduced antioxidant capacity, sustained inflammation, sympathetic activation, and endothelial dysfunction. Preclinical evidence is limited and mostly derives from in vitro scratch assays. It shows that IH delays wound closure, downregulates HIF-2α and VEGF, and shifts macrophages toward a pro-inflammatory phenotype. Clinical data are also limited and heterogeneous. In diabetic foot ulcers, high OSA risk doubled the risk of poor healing. Improved ulcer healing after CPAP has been described only in a small case series. Conclusion Given its high prevalence and underdiagnosis, OSA may be an overlooked and potentially modifiable factor in impaired wound healing.

Obstructive sleep apnea (OSA)-induced hypoxia modulates inflammatory mediators associated with atherosclerosis and cardiovascular diseases. ICAM-1, VCAM-1, TNF-α and IL-6 are involved in atherogenesis, but their expression in the aortic walls of OSA patients remains unknown. This study aimed to determine the relationship between OSA severity and inflammatory markers expression in aortic tissue from patients undergoing coronary artery bypass grafting (CABG). This study included 46 patients who underwent CABG. OSA severity was assessed using the WatchPAT™ home sleep apnea test, classifying patients into control and mild (0 < AHI < 15) and moderate-to-severe (AHI ≥ 15) OSA groups. Aortic wall samples were collected intraoperatively, and ICAM-1, VCAM-1, TNF-α and IL-6 expression was evaluated using immunohistochemistry. Statistical analysis compared protein expression across OSA severity groups. Compared with control and mild OSA, in aorta of the moderate-to-severe OSA group, significant differences for ICAM-1 (p = 0.001) and VCAM-1 (p = 0.006) expression were demonstrated. This study provides novel evidence of significantly increased ICAM-1 and VCAM-1 expression in the aortic walls of patients with moderate-to-severe OSA. No statistically significant differences were observed for TNF-α and IL-6. Our findings offer a rationale for integrating vascular inflammation markers into cardiovascular risk stratification in OSA. They also support the concept of OSA as a systemic inflammatory disorder, with tangible effects on large-vessel morphology.