Hyperbaric Oxygen Therapy (HBOT) is the medical use of oxygen at higher level than atmosferic pressure.
It uses a special chamber, called pressure chamber, in which the amount of oxygen is higher than in normal condition.
The air pressure inside a pressure chamber can be variable depending on chamber type. In a hard shelled pressure chamber it can reach 6 bars, while in soft chambers it can rise of 0.3-0.5 bars above atmosferic pressure. Hard chamber are expecially used treating decompression sickness.
Moreover it requires a device delivering 100% oxygen. This is useful in order to raise oxygen levels carryed by red blood cells and plasma.
HBOT was developed as a treatment for decompression sickness and gas embolism.
HBOT can help healing more quickly wounds, expecially infected ones.
It is used treating:
• bone infections
• necrotizing soft tissue infections
• radiation injuries
• gas gangrene
• Wounds not healed by other treatment (i.e. diabetic ulcer or serious circulation problems)
Unfortunately pressure chamber are not widespread and few hospitals own it.
For more information about using HBOT.
Complications and concerns
There are risks associated with HBOT, similar to some diving disorders. Pressure changes can cause a barotrauma in the tissues surrounding trapped air inside the body, such as the lungs, behind the eardrum, inside paranasal sinuses, or dental fillings. Breathing high-pressure oxygen may cause oxygen toxicity. Temporarily blurred vision can be caused by swelling of the lens, which usually resolves in two to four weeks.
Diabetic foot ulcer
Diabetic foot ulcer is a major complication of diabetes mellitus. If not treated it may cause lower-leg amputation.
There are many mechanism underneath diabetic ulcer.
• Altered metabolism: metabolic disorder consequent to diabetes mellitus causes an increased presence of aldose sugar. This fact leads to uncontrolled glycosylation of proteins and lipids, that accumulate over cell membrane. These products are called Advanced Glycation Endproducts (AGEs) or Amadori products and they cause ahterosclerosis due to increasing stiffness resulting from AGE-AGE intermolecular covalent bonds or cross-linking.
• Presence of AGEs modifies structure and function of many tissues
• AGEs activate receptors for AGEs (RAGE) that causes upregulation of the transcription nuclear factor k-b (nfkb)
• Soluble AGEs activate monocytes leading to inflammation and monocyte migration
• AGEs block endothelial nitric oxide synthase (eNOS) activity and causes production of Reactive Oxygen Species. Also NO regulates angiogenesis and plays a major role in wound healing, that is therefore blockedin diabetes patients.
More information about AGEs and it's effects can be found here
HBOT in the diabetes
An astonishing study of 2004 demonstrated that HBOT significantly reduces the risk of major amputation and may improve the chance of healing at 1 year. It has been recently re-confirmed by a new study of the European Society for Vascular Surgery.
Also the European Foot and Ankle Society confirmed the usefullness of HBOT in diabetes patient with ulcer with impaired cicatrization.
But why the HBOT is so useful?
It has been discovered that HBOT rises IGF-1 levels in the damaged tissue, contributing healing diabetic wounds.
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Growth factors influence the healing process, and among these, insulin-like growth factor (IGF) has been shown to stimulate keratinocyte proliferation in vitro. Existing evidence indicates that IGF-1, a proinsulin-like growth factor that modulates tissue growth and repair, and IGF-binding proteins (IGFBPs) play important roles in glucose homeostasis in diabetic patients. A lack of IGF-1 expression within the basal layer and fibroblasts may contribute to retarded wound healing in diabetes mellitus patients.
Insulin and insulin-like growth factor (IGF-1) play important roles in vascular biology. Both hormones regulate vascular tone, in part by decreasing vasoconstrictor responses to agonists, such as angiotensin II, norepinephrine, and vasopressin.
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Furthermore HBOT mobilizes stem cells in the tissue from the bone marrow by a nitric oxide (NO) dependent mechanism.
In contrast to this evidences there are some findings that go against this thesis. First of all the main problem with HBOT is the production of Reactive Oxygen Species (ROS). In fact the hyper-oxygenation of the tissues may produce ROS, also because of the inflammatory state of the tissue. The inlammation attracts monocyte on the site and hyperoxygenation, combined with the lack of function of NO Synthase (eNOS) results in a excessive production of ROS. Nonetheless the same and other studies highlith that HBOT for short period (i.e. two weeks) is truly effective.
Besides there are few studies involving high number of population, leading to uncertainty of effectiveness. Also some studies are doubtful about HBOT, expecially concerning levels of ischemia-modified albumin and blood glucose levels.
Finally HBOT is used as an adjuvant treatment in multistep and multidisciplinar cases, such as Fournier's gangrene in a patient with unknown type II diabetes: surgery, hyperbaric oxygen, and vacuum-assisted closure therapy.
On one hand the lack of large studies above HBOT doesn't allow implementing HBOT in routine practice. On the other hand actually HBOT can be used as an adjuvant treatment in non-healing wounds.
Moreover HBOT is expensive, if hospital doesn't own it.
Therefore new and more confident studies must be done before widesp