Definition and Causes

Chronic, complex, or problem wounds are skin ulcers or sores that do not heal without special treatment. Wounds that fail to heal in three months are usually considered chronic. Some take years to heal or never do.

Represent a significant and growing challenge to our healthcare system. The incidence and prevalence of these wounds are increasing in the population resulting in growing utilization of healthcare resources and dollars expended.

Common chronic wounds include venous ulcers (leg), arterial ulcers (foot), diabetic ulcers (leg and foot), and pressure ulcers (bedsores on elbows, back, ankles, hips, and heels).

Require a healthy, oxygenated wound bed to heal.

A lack of sufficient oxygen (hypoxia) in the wound bed slows or stops the normal healing process. Healing is notably difficult in patients with poor general or circulatory health.

Diabetes, in particular, may inhibit wound healing and increase the risk of infection and amputation.

Wounds resulting from trauma, surgery, burns, skin grafting, and adiation therapy may also become problem wounds.

Chronic wounds are especially prone to serious bacterial infections that threaten life and limb.

Factors make a wound to be problematic and thus chronic;

General Factors

Local Factorsς


Hypoxia(lack of oxygen



Advanced age

Foreign bodies


Arterial insufiency


Venus insufiency


Local toxins


chemotherapeutic drugs



Treatment with Hyperbaric Oxygen Therapy

Hyperbaric oxygen therapy (HBOT) is an effective adjunct to traditional wound care therapies, including topical cleaning; surgical removal (debridement) of dead skin and tissue; application of dressings, ointments, and biologics; and use of compression boots or stockings, vacuum or negative pressure wound therapy (NPWT) pumps, ultrasound, laser, and other emerging technologies. HBOT helps repair wounds and enhance healing by improving blood circulation, encouraging the formation of new capillary blood vessels (angiogenesis), supplying more oxygen to tissue in the wound bed, and stimulating the growth and distribution of stem cells.

Hyperbaric oxygen also helps kill the anaerobic bacteria that cause some of the worst infections in chronic wounds.

Evidence for HBOT is especially strong in diabetic foot ulcers classified Wagner Grade 3 or higher, for which hyperbaric oxygen is widely considered standard therapy.

Undersea and Hyperbaric Medical Society

Mechanisms of HBO2

Regardless of the primary etiology of problem wounds, a basic pathway to non-healing is the interplay between tissue hypoperfusion, resulting hypoxia, and infection. A large body of evidence exists which demonstrates that intermittent oxygenation of hypo-perfused wound beds, a process only achievable in selected patients by exposing them to hyperbaric oxygen treatment, mitigates many of these impediments and sets into motion a cascade of events that leads to wound healing.

Hyperbaric oxygenation is achieved when a patient breathes 100% oxygen at an elevated atmospheric pressure. Physiologically, this produces a directly proportional increase in the plasma volume fraction of transported oxygen that is readily available for cellular metabolism. Availability of substrate for oxygen dependent enzymatic reactions critical to repair and resistance to infection is even more important than normalization of metabolic rate. Furthermore, oxidants appear to be among the most important signals that control the healing process, and this may be another mechanism for the benefits of HBO2T in hypoxic wounds. Arterial PO2 elevations to 1500 mmHg or greater are achieved with 2 to 2.5 atm abs with soft tissue and muscle PO2 levels elevated correspondingly. Oxygen diffusion varies in a direct linear relationship to the increased partial pressure of oxygen present in the circulating plasma caused by hyperbaric oxygen therapy.

This significant level of hyperoxygenation allows for the reversal of localized tissue hypoxia, which may be secondary to ischemia or to other local factors within the compromised tissue (eg, edema and inflammation).

In the hypoxic wound, hyperbaric oxygen therapy acutely corrects the pathophysiology related to oxygen deficiency and impaired wound healing. A key factor in hyperbaric oxygen therapy’s enhancement of the hypoxic wound environment is its ability to establish adequate oxygen availability within the vascularized connective tissue compartment that surrounds the wound. Proper oxygenation of the vascularized connective tissue compartment is crucial to the efficient initiation of the wound repair process and becomes an important rate-limiting factor for the cellular functions associated with several aspects of wound healing.

Neutrophils, fibroblasts, macrophages, and osteoclasts are all dependent upon an environment in which oxygen is not deficient in order to carry out their specific inflammatory or repair functions. Improved leukocyte function of bacterial killing and antibiotic potentiation, have been demonstrated. Suppression of synthesis of many bacterial toxins(55) occurs when tissue PO2 values are sufficiently elevated during treatment. Blunting of systemic inflammatory responses and prevention of leukocyte activation and adhesion following ischemic reperfusion are effects that may persist even after completion of hyperbaric oxygen treatment.

Stimulation of tissue growth supporting wound healing has also been demonstrated by a variety of mechanisms:

1) Vascular endothelial growth factor (VEGF) release is stimulated(60) and platelet derived growth factor (PDGF) receptor appearance is also induced.

2) Boykin has recently demonstrated persistent increases in nitric oxide in wound fluid in diabetic ulcers associated with increased granulation tissue formation and wound closure when patients are exposed to 20 hyperbaric oxygen treatments at 2.O ATA for 90 minutes.

3) Stem/progenitor cell release from bone marrow through a nitric oxide dependent mechanism occurs in patients receiving hyperbaric oxygen treatment for soft tissue and osteoradionecrosis. The population of CD34 cells in peripheral circulation doubled in response to single HBO treatment (2 ATA, 120 mins). Over course of 20 treatments circulating CD34 cells increased 8 fold, total WBC count unchanged.


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