Patients with chronic non-healing wounds often have major co-morbidities such as diabetes and cardiovascular diseases \[1\]. Obstructive Sleep Apnea (OSA) is present in up to 24% of middle-aged adults \[2\], and is far more prevalent in patients with existing cardiovascular disease \[3\]. Patients with OSA are at increased risk of developing diabetes l \[4\]. OSA is an established cause of hypertension\[5\], and has an estimated prevalence of 40% in all patients with hypertension \[6-8\]. Similarly a strong association exists between OSA, coronary artery disease \[6, 7\] and stroke \[8\]. OSA may be present in over 50% of patients with heart failure \[9\]. Patients with chronic non-healing wounds stand to benefit from identification and treatment of severe co-morbidities such as OSA. Such identification and treatment of OSA will impact the survival of these patients \[10, 11\], and may also contribute to improved morbidity via impacting wound healing.
Several unexplored links exist between OSA and wound healing. OSA is a disorder of intermittent hypoxia and is associated with increased oxidative stress \[12\]. Humans with OSA and animal models of intermittent hypoxia developed impaired vascular function and nitric oxide deficiency. Patients with OSA have impaired endothelial function even in the absence of clinically apparent cardiovascular disease \[13-15\]. Increased sympathetic activity and episodic pressor response are well documented in OSA. Patients with OSA have increased vascular tone and baseline vasoconstriction \[16\]. Impaired vascular reactivity to hypoxia was also demonstrated in animal models exposed to 2 weeks of intermittent hypoxia\[17\]. Therefore, in patients with chronic non-healing wounds, OSA is likely to further complicate the healing process.
OSA as a disorder of oxidative stress and vascular impairment is most likely an important co-morbidity in patients with non-healing wounds. Other potential mechanisms of interaction are the inflammatory response associated with OSA
