Hyperbaric Oxygen Therapy can help to heal bone disorders by stimulating both the osteoclasts and the osteoblasts. This helps and leads to the re-absorption of dead bone and the creation of new bone. In addition, HBOT stimulates the production of new blood vessels, so that the growing bone receives a steady supply of nutrients, including oxygen. The increased blood vessel network that HBOT yields does two other things: it helps support the function of the osteoclasts, and brings infection fighting white blood cells to the area.
Osteomyelitis is a bacterial infection that usually involves both the outer layers of the bone and the inner bone marrow. Staphylococci, is a common form of bacteria that can cause infections ranging from pimples to meningitis. Staphylococci are an anaerobic (oxygen hating) bacteria, making HBOT ideal for controlling its spread.
- Chronic osteomyelitis may follow an acute form or may develop over time; this is also when the acute form is not completely cured by treatment.
- Long–term Osteomyelitis which in some cases continues for years.
- Refractory osteomyelitis is a term referring to the condition of bone infection that did not respond to either surgical or antibiotic therapy
Part of the difficultly in treating osteomyelitis lies in the fact that it causes a lack of oxygen in the tissues. HBOT, by providing forced oxygenation, helps fight this disorder along with antibiotic therapy and or surgical intervention. Hyperbaric Oxygen Therapy helps preserve healthy bone, restore, and help build new bone and helps with the immune system. In some cases, in both bones and wounds, HBOT draws a clear line by which the surgeon can aid in the removal of dead or diseased bones. These types of infections can occur sometimes in the extraction of a tooth.
A good three-part treatment for bone infections includes the use of antibiotics, surgery to remove the dead bone, and HBOT as a supporting or adjunct treatment. There are some surgeons who are using HBOT before and after surgery.
Hyperbaric Oxygen in the Treatment of Controlled Laser Induced Thermal Burns
Hyperbaric oxygen therapy (HBOT) has established itself as an adjunctive treatment for thermal burns. The physiological damage of these burns is comparable to the thermal burns induced by CO2 Laser resurfacing. Laser resurfacing is a procedure for indications such as sun damage, telangiectasias, eliminating facial rhytides or wrinkles. The elective nature of the procedure allows for any patient with the will power and the financial freedom to undergo this procedure. The purpose of this article is to evaluate and compare thermal burns and controlled laser resurfacing thermal burns, their definitions, treatments and the possible adjunctive hyperbaric oxygen treatments. The subject of adjunctive hyperbaric oxygen therapy in the treatment of controlled laser induced thermal burns will also be compared, seemingly due to its role in the treatment of thermal burns.
Laser resurfacing has recently become the vogue for reducing or eliminating facial rhytides or wrinkles. The evolution of this process has been a long time in coming. Previously, CO2 lasers were used for cutting and destruction of tissues. This is a less controlled use of laser energy. The advent of the computer pattern generator revolutionized the laser industry. Now instead of physician judgment of how long and where to aim the laser, the computer would selectively irradiate the chosen tissue in a uniformly repeatable fashion for a specified period of time. This revolutionized the laser industry and brought about great research into laser biophysics. Thus in the early 1980?s, Anderson and Parrish developed the theory of Selective Photothermolysis (Anderson RR, Parrish JA; Selective photothermolysis; Precise microsurgery by selective absorption of pulsed radiation. Science 220:524, 1983) this theory states that the effects of a laser begin by energy being absorbed at specific sites called chromophores. The chromophore for a CO2 laser is water. Consequently, exposure to a CO2 laser will superheat the water molecule within the cell and thus cause the cell to vaporize. The distribution of laser heating in the skin is not only determined by the depth of laser penetration but also over the period of time that the laser energy was distributed.
Controlling these attributes allows us to ablate tissue and cause a controlled thermal burn, which results in a controlled scarring process that appears to eliminate wrinkles. A certain portion of energy extends into the underlying dermis by thermal conduction. Consequently we are not resurfacing the face with new tissue, we are allowing a controlled scar to evolve. Scars shrink over time, a process called contracture. This controlled contracture is what gives the appearance of youthful un-wrinkled skin.
Thermal effects on tissue are both time and temperature dependent:
42-45 degrees C-reversible protein and membrane changes
50-85 degrees C-structural protein denaturization
75-80-irreversible collagen coagulation
Greater than 100-vaporization of tissue water, then ablation and carbonization.
Complications of CO2 Laser Resurfacing
Laser surgery has exploded in the past decade, both in the number of indications for its use as well as the number of types of lasers. As with all surgical modalities, excellent results are tempered by the existence of complications such as those listed below.
Postoperative hyperpigmentation can be seen after almost any cutaneous laser procedure, regardless of type. It is more common in patients with darker skin types and is, in the vast majority of cases, a temporary side effect that responds to time and topical bleaching therapy. It is relatively common after CO2 laser resurfacing, where it lasts for an average of 3-4 months.
Postoperative hypopigmentation is also possible, particularly after pigment-specific laser irradiation. In these situations, it is seen more commonly after multiple treatments and is more common in darker skin types. As with hyperpigmentation, this complication is often temporary, although permanent hypopigmentation has been seen. Delayed permanent hypopigmentation has been recognized as a complication particular to CO2 laser skin resurfacing.
Blister formation (or vesiculation) is due to epidermal thermal damage induced by the laser. Explanations for its development include use of excessive laser fluencies or inadvertent absorption of laser energy due to the increased presence of an epidermal chromophore (e.g., melanin in a tan). The concomitant use of tissue cooling (through a contact chill tip or cryogen spray) serves to protect the epidermis from excessive thermal damage during laser irradiation.
This undesirable effect is also due to laser-induced epidermal damage (see blistering). Without appropriate postoperative care, crusting is inevitable after cutaneous laser resurfacing procedures.
Milia are often seen as a normal event in the postoperative course of patients who have undergone CO2 or erbium laser skin resurfacing. Their development may be reduced by application of topical tretinoin or glycolic acid.
This is perhaps the most dreaded of laser complications and was relatively common with continuous wave lasers. The risk of scarring with more recently developed pulsed and Q-switched lasers utilizing the principles of selective photothermolysis is far less, but remains possible. Whether atrophic or hypertrophic in type, scarring is always due to excess damage to the dermis. This may be the result of direct laser-induced thermal damage or may arise from complications such as postoperative infection. In general, risk of scarring is low with pigment-specific lasers, non-continuous wave vascular lasers and pulsed hair removal laser systems. Cutaneous laser resurfacing (both CO2 and erbium) carries the highest risk of scarring because of the intended destruction of dermal tissue as well as the increased risk of infection in the de-epithelialized skin. Factors such as the number of passes delivered and energy used may affect the risk of scarring, this complication may be seen even in the hands of the most experienced surgeon.
Definition of Thermal Burns
A thermal burn is an injury caused by exposure to heat sufficient to cause damage to the skin, and possibly deeper tissue. Most thermal burns are caused in one of the following ways, FLAME, HOT LIQUIDS, HOT OBJECTS, FLASH INJURIES and SUNBURN. The burn wound is a complex and dynamic injury characterized by a zone of coagulation, surrounded by an area of stasis, and bordered by an area of erythema. Depending on the severity of the thermal burn the zone of coagulation or complete capillary occlusion may progress by a factor of 10 during the first 48 hours after injury. Edema formation is rapid in the area of injury but also develops in distant, uninjured tissue. There are changes also occurring in the distant microvasculature where red cells aggregate, white cells adhere to venular walls, and platelet thromboemboli occurs. This is a progressive ischemic process which, when set in motion, may extend the damage dramatically during the early days after injury. The continuing tissue damage seen in thermal injury is due to the failure of the surrounding tissue to supply borderline cells with oxygen and nutrients necessary to sustain viability. The impediment of circulation below the injury leads to desiccation, as fluid cannot be supplied via the thrombosed or obstructed capillaries. Topical agents and dressings may reduce, but do not prevent, desiccation of the burn wound and the inexorable progression of the injury to deeper layers. Regeneration cannot take place until equilibrium is reached; hence, healing is retarded. Prolongation of the healing process may lead to excessive scarring. Hypertrophic scars are seen in 4 per cent of patients taking 10 days to heal, in 14 per cent of patients healing in 14 days or less, in 28 per cent of patients taking 21 days, and up to 40 per cent of patients taking longer than 21 days to heal. Rational for Hyperbaric Oxygen Therapy in Thermal Burns
Rational for Hyperbaric Oxygen Therapy in Thermal Burns
Initial burn therapy must be directed to minimizing edema, preserving marginally viable tissue, enhancing host defenses, and promoting wound closure. Adjunctive hyperbaric oxygen therapy can attack these problems directly, maintaining microvascular integrity, minimizing edema, and providing the essential substrate necessary to maintain viability. The beneficial effects of HBOT are vasoconstriction & fibroblast proliferation.
Effects of Hyperbaric Oxygen on Thermal Burns
The postulated mechanisms of a beneficial effect of hyperbaric oxygen on burn wounds are decreased edema due to hyperoxic vasoconstriction, increased collagen formation, and improved phagocytic killing of bacteria. In a trial comparing burn treatment with and without hyperbaric oxygen in 16 patients, the healing time was significantly shorter in the group receiving hyperbaric oxygen. Rationale for Hyperbaric Oxygen Therapy in Laser Induced Thermal Burns. The mechanisms of insult in a controlled laser induced thermal burn are similar to the insult in a thermal burn. The controlled laser induced thermal burn has a less dramatic insult due in part to its controlled nature. The extent of thermal damage is generally from 200 to 400 microns, sufficient enough to be classified as a partial thickness burn, but could be less with HBOT treatments early on after the surgery. The same pathophysiology of the thermal burn applies to laser burns, the edema, erythema but the ischemia is less severe.
Hyperbaric oxygen treatment of the controlled laser induced thermal burn has shown a reduction in edema, erythema and promotes faster wound healing. Because the severity of the burn is not considered 20 per cent of the body or life threatening as specified in most HBOT literature as an indication for treating the thermal burn wound, the benefits seen in the hyperbaric oxygen treatment of the thermal burns are the same benefits seen in the treatment of controlled laser induced thermal burns. Treatment protocols for a less severe thermal burn like the laser induced thermal burn is anywhere from 5 to 10 treatments postoperatively. Each HBOT treatment is 90 minutes at 2 atmospheres (equal to 33 feet underwater). It has been observed that the patients whom elect to undergo the hour and a half HBO treatment protocol post laser resurfacing have healed 30 to 40 percent faster than those that don’t do the treatments, and the chances for hypertrophic scarring and other complications are reduced by as much as 80 percent.
Although the treatment for the controlled laser induced thermal burn is not an approved indication by insurance companies for hyperbaric oxygen therapy, the fact remains that the patient can benefit from the HBOT treatments. Insurance coverage is a moot point in the reimbursement for this indication due to its elective nature (laser resurfacing is an elective procedure). The research has been extensive in the adjunctive HBOT treatment for thermal burns and should pass scrutiny based on its merits alone. The fact is that the treatment for thermal burns has itself not been widely accepted due to the lack of general understanding about Hyperbaric Oxygen Therapy and its benefits. This lack of understanding and ignorance hinders the progression of further research and usage of the treatment for indications that obviously benefit from its adjunctive use.
Remember hyperbaric oxygen therapy is not employed to replace any other treatment modalities but to be used adjunctively with them to get the best possible outcome for the patient. The hyperbaric oxygen therapy not only limits the doctor’s liability but also cuts the healing process for the patients thereby shortening the number of post-operative office visits.
(From Hyperbaric Medicine Today. www.hbomedtoday.com)
HBOT has been shown to reduce recovery time of various soft-tissue injuries and bone fractures. At least 12 professional NBA, NHL and NFL teams (including the New York Giants and the Dallas Cowboys) own or lease hyperbaric oxygen chambers for treating their players.
A concern expressed by some physicians is that HBOT will stimulate the growth of cancer. Experimental animal data by Matko Marusic, Ph. D. showed that HBOT given after inoculation of cancer cells decreased the take of the cancer cells. Again, the thousands of patients treated with the Marx protocol have demonstrated a lower recurrence of cancer in patients who received HBOT as part of their reconstructive process than those who had only antibiotics and surgery.
Based on the data above, HBOT has a significant role in cancer care but it has been under utilized except for reconstruction of head and neck cancer. In the future, the value of HBOT in cancer care should be the basis for expanded use of HBOT in care of the cancer patient.
Fatigue is a common complaint of the cancer patient. It may be due to the cancer itself or from cancer treatments. Results with HBOT have been reported in patients with migraine and chronic fatigue syndrome. Therefore, it seems probable the fatigue of the cancer patient would also respond to HBOT.
HBOT In Cancer Care Anemia
Anemia is a frequent result of cancer and cancer treatment. The anemia of cancer and cancer treatment should also respond well to HBOT. The ability of HBOT to stimulate the bone marrow is the rationale for use of HBOT in acute blood loss anemia. Chronic anemia can also respond well to HBOT. Addition of HBOT to erythropoetin treatment of anemia should increase and speed response. 34-year-old female with Lupus who developed osteomyelitis of distal 5th finger. The surgical recommendation was amputation of the finger. The osteomyelitis was cured with antibiotics and 60 days of HBOT at 2ATA for 2 hours per day. Her hemoglobin increased 3.8 grams and the patient had her first period in 5 years. MUCOSITIS AND ESOPHAGITIS Mucositis and esophagitis are debilitating complications of chemotherapy and radiation therapy with a higher incidence in concurrent or sequential treatment programs. Recent reports indicate a complicating factor is a superimposed pseudomonas infection. HBOT speeds healing, reduces edema and is very effective against pseudomonas infection. Amifostine (Ethyol) and recombinant human kevatinocyte growth factor (rhukgforkgf) are reported as treatments for mucositis and esophagitis. Adding HBOT to these treatments should significantly improve response. Therefore, the use of HBOT for muscositis and esophagitis should also be considered as acute ucositis and esophagitis respond well to HBOT. 54-year-old diabetic who ruptured his Achilles tendon. Post-operatively, he developed pseudomonas infection that progressed in spite of antibiotics. Achilles tendon is shown in infected wound before HBOT.
At Start of HBOT Development of granulation tissue after 20 treatments of HBOT at 2ATA 2 hours per day. Response at 2 Weeks Skin graft doing well. HBOT was continued . Patient received 120 HBOT treatments. At one year follow-up there was 100% take of graft. Prior to HBOT patient had one to two TIA’s per month. Post HBOT, no TIA’s for one year.
The use of HBOT as an adjunct to radiation therapy was tried 40 years ago. At that time, the radiation therapy was given while the patient was at pressure in the hyperbaric oxygen chamber. As both the normal cells and the cancer cells were hyperoxygenated, the expected increase in cancer control and decrease in modality did not occur. Twenty years ago, I started using HBOT prior to the radiation therapy treatment for difficult cases. This technique of HBOT immediately before the radiation therapy worked well with my patients . In a 1999 article, Drs. Kohshi, Kanugita, Kinoshita and Abe from Japan, reported using this technique of HBOT before radiation therapy. They found a 50 percent increase in survival for brain tumor patients using the pre-radiation HBOT treatment.
Using HBOT before the radiation therapy treatment permits the normal tissue to return to standard oxygenation while the less vascular cancer will still have an increased oxygen level as does the slow healing wound post HBOT. It is well documented that good oxygenation is needed for full response to a dose of radiation therapy.
34-year-old white female with synovial cell carcoma of chest wall. Patient was given 4,000 rads to chest wall with HBOT 2 hours at 2ATA just before each radiation therapy treatment. At one month after completion of radiation, patient had wide surgical excision and skin graft followed by an additional 20 days of HBOT post graft. Graft take was 100 percent as shown at one-year post graft. Eighteen years post treatment, there is no recurrence.
References available upon request. e-mail:
Chemo Brain Response To HBOT
A 56-year old woman was diagnosed in 1993 with breast cancer. She had a lumpectomy followed by six weeks of radiation therapy and six months of chemotherapy with Cytoxan, methotrexate, and fluorocuracil. Tamoxifen therapy was given for five years. Shortly after starting chemotherapy, she noted a gradual and progressive memory impairment with confusion, poor ability to recall recent events and understand information provided to her. She had a tendency to misplace her possessions and lost interest in many of the activities she had participated in previously, including playing bridge. Her reading comprehension deteriorated and she no longer was able to cook many of the dishes that she had prepared in the past. Because of the cognitive defect, she had to stop working in 1996. The patient was evaluated for HBOT on 04-05-02 . She received 20 treatments of hyperbaric oxygen therapy (HBOT) for 1 hour at full pressure of 1.5 ATA. At her last evaluation on 07-08-02 , the patient reported that there had been significant improvement in her memory and she was no longer in a “fog”. There was significant improvement in her ability to analyze and think out tasks that she needed to perform which she could not do before HBOT. Due to her memory improvement she has been able to return to work for the first time in six years.
Pseudomonas Response To HBOT Hand-Foot Syndrome From 5-FU, Doxorubicin, Docetaxel And Capecitabine
An adverse reaction from 5-FU, Doxorubicin, docetaxel and Capecitabine chemotherapy has been termed the hand-foot syndrome (HFS) and is also called palmar plantar erythrodysesthesia (PPE). HFS/PPE is a frequent toxic reaction which causes a painful erythema, often preceeded by paresthesia in the palm of the hands and sole of the feet. Histology shows mild spongiosis, scattered necrotic dyskeratotic keratinocytes and vascular degeneration of the basal layer of the skin. Dermal changes include dilated blood vessels, papillary edema and pervascular lymphohistiocytic infiltrate. In some severe cases there has been loss of hands and feet. Treatment has been drug withdrawal, hyperbaric oxygen therapy, and supportive topical wound care. Based on physiological effects of HBOT, which are vasoconstriction, edema reduction, stimulation of capillary formation and increased oxygenation, the use of HBOT might significantly decreases the morbidity of HFS/PPE syndrome caused by 5-FU, Doxorubicin, docetaxal and Capecitabine. To help you discover what Hyperbaric Oxygen Therapy can do for you, for a limited time, Dr. Spiegel will provide a free assessment to determine if you would benefit from this treatment.
To schedule a hyperbaric oxygen therapy consultation, give our office a call