By Paul G Harch MD
Hyperbaric oxygen therapy (HBOT) was first defined as a drug in 1977 by Gottlieb (1). Unfortunately, this critical definition has been long forgotten and substitute definitions have mis-characterized HBOT as a therapy for "certain recalcitrant, expensive, or otherwise hopeless medical problems."(2) This mischaracterization has resulted in a confusing collection of different lists e.g., CMS, UHMS Accepted Indications, and international lists(3), of seemingly unrelated reimbursable diagnoses (chronic refractory osteomyelitis, air embolism, cyanide poisoning, compromised flaps and grafts, carbon monoxide poisoning, acute stroke, etc) supported by widely varying amounts of basic science and clinical evidence. In 1999 the drug definition of HBOT was refined and restated as the use of greater than atmospheric pressure oxygen as a drug to treat basic pathophysiologic processes and their diseases (4). With that definition the above lists could now be understood as cohesive sets of diagnoses connected by HBOT effects on the acute and/or chronic underlying pathophysiology common to the diseases. Furthermore, the definition suggested and argued for the application of HBOT to additional diseases that shared this pathophysiology. The 1999 drug definition of HBOT will be used in this paper to argue for HBOT effectiveness in the treatment of infected diabetic foot wounds, and hence, CMS reimbursement for the same. The argument will be constructed by identifying the underlying pathophysiology in diabetic foot wounds, presenting the evidence for the beneficial effects of HBOT on this pathophysiology, demonstrating a similar benefit in patients with diabetic foot wounds, and then showing the risk/benefit and cost/effectiveness evidence for HBOT in diabetic foot wounds. This argument will lead to the conclusion that CMS coverage of HBOT should be extended to diabetic foot wounds.