Meleney’s Ulcer is an antiquated term used to describe a rare progressive cutaneous infection.
Dr. Frank Meleney and Dr. George Brewer described this syndrome in 1926 as a necrotizing bacterial infection created by the synergism between aerophilic and anaerobic/microaerophilic bacteria. The condition is now called Progressive Necrotizing Infection or, commonly, “flesh-eating bacteria.”
The diagnostic criteria include a slowly progressive, superficial necrotizing process, evidence of a variety of anaerobic, amoebic, and/or micro-areophilic organisms, hypoxic wound environment and microvascular thrombosis* in a full thickness ulcer.
* the formation of a blood clot in a blood vessel obstructing blood flow and oxygen delivery to the tissues. When a vessel is injured, platelets and fibrin try to fix the damage by forming clots to prevent blood loss. However this can happen without an initial injury due to other conditions. If clotting is too severe, blood flow to the tissue is reduced or halted causing hypoxia and infarction (cell death due to lack of oxygen). A clot may break off from the vessel, causing a stroke in the brain tissue, myocardial infarction in the heart, and other complications such as peripheral vascular occlusion in the limbs.
Some diabetic foot ulcers meet the criteria for this disease, but not all diabetic ulcers are automatically PNI. While diabetic ulcer wounds are hypoxic and have microvascular thrombosis, they must also have an expanding margin to be considered PNI.
The use of HBOT in this condition is very well documented in the medical literature and is considered as adjunctive to standard surgical and antibiotic therapy. HBOT inhibits growth of anaerobic or micro-aerophilic organisms, enhances neutrophils function and increases the efficacy of certain antibiotics. Once the spread of the necrotic process has been stopped, HBOT may promote healing by stimulating angiogenesis and granulation tissue formation.