References
Healing of chronic sickle cell disease-associated foot and ankle wounds using transdermal continuous oxygen therapy
Abstract
Objective:
Sickle cell disease (SCD) is a complex cause of capillary stasis that can lead to lower extremity venous ulcers. Since SCD is characterised by impaired oxygen delivery that can be exacerbated by lower extremity venous stasis, we sought to determine if direct delivery of oxygen to a lower extremity ulcer associated with SCD could augment healing.
Method:
We performed a pilot study of a portable device that delivers oxygen directly to the wound site to assess this possibility. The device was assessed in a single patient with three longstanding wounds of the lower extremities associated with SCD: the lateral right ankle, the medial aspect of the distal left leg, and the dorsal left foot. The left leg and left foot wounds received 15 weeks of treatment each.
Results:
Both left lower extremity wounds healed, and neither wound has relapsed in the 42 months since the treatment was completed. At 36 months from the completion of treatment, the patient presented to the hospital with renal failure, and with the 27 days of complete bed rest and wound elevation, the right ankle wound shrunk to 55% of the original wound surface area. Transdermal oxygen appears to have assisted in healing and to have provided a sustained benefit that has delayed relapse of the two SCD-associated leg ulcers that received an extended course of treatment. Similarly, complete bed rest appears to aid in the healing of SCD-associated leg ulcers. Further study is needed to determine the mechanism of action and the optimal method of use of the transdermal continuous oxygen delivery device for SCD-associated lower extremity ulcers.
Venous stasis-related ulcers have been estimated to affect up to 1% of the population in the US, resulting in an estimated cost of approximately $1 billion spent annually on the medical and surgical treatment of these ulcers.1 One of the comorbidities that can complicate treatment of venous stasis ulcers is sickle cell disease (SCD), an inherited disorder that is characterised by the presence of haemoglobin S (HbS). HbS is a genetic variant of haemoglobin that tends to polymerise when deoxygenated, which changes the flow characteristics of the blood and leads to many of the complications of SCD, including the formation of lower extremity ulcers. These ulcers are extremely painful and disabling, and can be relatively common: one cross-sectional study showed that the point prevalence of leg ulcers is 2.5% and the incidence is 10 per 100 person years in SCD patients above the age of 10 years old.2 The exact pathogenesis of SCD-associated lower extremity ulceration is unclear, but venous stasis and the associated hypoxia of the distal leg are thought to be contributing factors.3 When HbS releases its oxygen to the tissues, the resultant hypoxia in the capillary triggers HbS polymerisation. HbS polymers then distort the red blood cells into a sickled shape. This sickled shape then increases blood viscosity and decreases flow velocity, which causes capillary stasis and tissue ischemia leading to tissue necrosis and impaired wound healing.4
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