Arterial gas embolism is a major cause of death in diving in which the initiating cause (pulmonary barotrauma) usually goes undetected. Caused most often by the expansion of respiratory gases during ascent, it also may also occur when the breath is held during ascent from a dive, when there is local pulmonary pathology, when there is dynamic airway collapse in the non-cartilaginous airways and if there is low pulmonary compliance, particularly if this is not distributed evenly throughout the lungs. Boyle's law is the physical law controlling the event. Experimental evidence indicates that intratracheal pressures of about 10 kPa (4 feet or 1.22 metres of seawater pressure) is all that's needed for it to happen. Distention of the alveoli leads to rupture, alveolar leakage of gas, and extravasation of the gas into the arterial circuit.
Necrotising Soft Tissue Infection
Common names:Necrotizing fasciitis; Flesh-eating bacteria; Soft tissue gangrene; Fourniers Gangrene;
Necrotizing soft-tissue infection is a severe type of tissue infection that can involve the skin, subcutaneous fat, the muscle sheath (fascia), and the muscle. It can cause gangrene, tissue death, systemic disease, and death.
Delayed radiation injury to soft tissue and bone
Cancer treatment has improved significantly over the past decade. Although cure of the cancer is still the highest priority of treatment, cancer specialists have come to recognise the ever-increasing importance of quality of life to the cancer survivor.
One-half of the estimated 1.2 million new cases of invasive cancer will receive radiation therapy as a part of their cancer treatment. Side effects of this therapy can be very toxic, especially when combined with chemotherapy. Some people are more sensitive to radiation damage than others, and there are no reliable tests available as yet to identify those patients who will experience the worst side effects.
Radiation doses must be adequate to control the cancer otherwise there is no purpose in treating the patient. Most radiation cancer specialists or oncologists design their treatment protocols to give the best dose to control the tumor and still have no more than 5% of patients develop severe reactions to treatment.
Radiation side effects are generally divided into two categories.
First, there are those that happen during or just after the treatment, called acute reactions.
Second, there are those that happen months or even years after the treatment, called chronic complications. The acute side effects almost always resolve with time and are treated in such a way as to address the patient's symptoms. For example, when a patient has a cancer of the mouth or throat, it becomes very difficult for the patient to eat during and just after treatment because the lining of the mouth and throat becomes raw and painful.
The more chronic complications are usually caused by the interruption of nutrients (specifically oxygen) passing through blood vessel walls in the affected area. This is caused by a process of hardening of these vessel walls as a secondary effect of the radiation. This vessel wall hardening does not allow for the oxygen to pass through to the tissues that require oxygen to repair themselves or indeed in severe cases for tissue survival. Hyperbaric oxygen has been shown to re-grow new blood vessels in the affected area (to about 80% of normal) thus restoring the tissue's ability to heal.
Selected problem wounds
The definition of a problem wound is one which fail to respond to established medical/surgical management in an appropriate timeframe. Depending on the wound size, an appropriate time to heal would be approximately 1 month. These wounds usually present in compromised hosts with multiple local and systemic factors which inhibit tissue repair. These include:
Compromised Amputation Sites
Non-healing Traumatic Wounds
Vascular Insufficiency Ulcers
Regardless of etiology, the basic mechanism of non-healing wounds is an interplay between varying degrees of tissue hypoperfusion and infection. All have the underlying problem of tissue hypoxia and its sequela as common denominators. Tissue oxygen tensions in or near such wounds usually measure below 20 mmHg. In a hypoxic environment, wound healing is halted by decreased fibroblast proliferation disagree - don’t change, collagen production and by capillary angiogenesis. Hypoxia also impairs oxygen-dependent intracellular leukocyte bacterial killing of the most common aerobic organisms found in wound infections and creates the ideal environment in which anaerobic and microaerophilic organisms flourish.
RATIONALE: Hyperbaric oxygen (HBO2) treatment provides a significant increase in tissue oxygenation in the hypoperfused, infected wound. This elevation in oxygen tension induces significant positive changes in the wound repair process. HBO2 promotes wound healing by directly enhancing fibroblast replication, collagen synthesis, and the process of neovascularization. Providing oxygen at the cellular level also increases leukocyte bacterial activity and has a direct lethal effect on anaerobic organisms. In summary, tissue oxygen tension influences the rate of collagen deposition, angiogenesis, and bacterial clearance in wounds. Hypoxia is deleterious and hyperoxia will enhance the wound healing process. HBO2 elevates oxygen tensions in ischemic and infected wound tissue. The greatest benefits are achieved in tissues with compromised blood flow and oxygen supply.
Gas gangrene, anaerobic infections, or necrotizing infections
This disease is caused when the bacteria in the family of Clostridium (e.g., Clostridium perfringens) infects the body tissue. Clostridium bacteria of this type can only live where there is little or no oxygen (i.e., anaerobic conditions). This occurs in damaged or injured tissues where the oxygen supply is low. It is called "gas" gangrene because the Clostridium bacteria release gas that causes swelling in the surrounding tissue.
Carbon monoxide poisoning
The pathophysiology of Carbon Monoxide (CO) poisoning includes:
Binding of CO to the hemoglobin molecule to form carboxyhemoglobin, reducing oxygen delivery to the tissues. Undefined cellular effects, as well as lipid peroxidation and cytochrome binding.
Produces a rapid dissociation of CO from hemoglobin (the half-time for elimination of CO is reduced from over 5 hours with air to 23 minutes).
Oxygen breathing at 3 atmospheres absolute (ATA) provides immediate delivery of dissolved oxygen in plasma in an adequate amount to support basic tissue metabolism, even when the amount of CO bound to hemoglobin is high.
Crush injury and other acute traumatic ischaemias including strokes
1. Crush injury is a diffuse traumatic injury involving two or more tissues with a gradient of injury and compromised blood supply. The primary insult is tissue ischemia and cellular hypoxia. Secondary effects of vasodilation at the pre-injury level lead to increased edema and further vascular compromise thus compromising the tissue's ability to handle infections.
Optimal response is evident if treatment is initiated within six hours of injury. Results are variable and are dependent on time to intervention. A literature review revealed benefit in approximately 60% of cases resulting in increased extremity survival, decreased tissue loss, and amputation at a more distal level.
Increases oxygen tension leading to greater capillary oxygen diffusion distances.
Produces a vasoconstriction that reduces edema formation.
Has an indirect effect of leukocyte enhancement and increased wound healing.
Decreases neutrophile adhesion & activation in the ischemic-reperfused tissue
2. There are two forms of stroke: ischemic - blockage of a blood vessel supplying the brain, and hemorrhagic - bleeding into or around the brain.
A stroke occurs when the blood supply to part of the brain is suddenly interrupted or when a blood vessel in the brain bursts, spilling blood into the spaces surrounding brain cells. Brain cells die when they no longer receive oxygen and nutrients from the blood or there is sudden bleeding into or around the brain. The symptoms of a stroke include sudden numbness or weakness, especially on one side of the body; sudden confusion or trouble speaking or understanding speech; sudden trouble seeing in one or both eyes; sudden trouble with walking, dizziness, or loss of balance or coordination; or sudden severe headache with no known cause.
Abscess formation in the brain can be a devastating complication of sinus infections or bone infections (osteomyelitis) of the skull. Occasionally, abscesses start from an infection from other parts of the body. Abscesses in the brain frequently occur in multiples. One of the problems in the treatment of brain abscesses is that surgical drainage of the abscesses is often required for cure.
Unfortunately, normal brain tissue surrounding the abscess may be unavoidably damaged by such surgery. Fine needle aspiration of the abscesses is being performed with greater frequency to avoid this problem.
Antibiotics are used for treatment, but they may not penetrate well into brain abscesses. Furthermore, white blood cells, which kill infecting bacteria, may not have enough oxygen to effectively eliminate the infection if they are functioning deep in the abscess at a distance from their normal blood supply. White blood cells require a minimum level of oxygen to kill bacteria.
Most intracranial abscesses are caused by anaerobic bacteria (bacteria that function optimally in low oxygen concentrations). Hyperbaric oxygen therapy raises the oxygen level in the region of the abscess, exposing the bacteria to levels which may inhibit or kill them, as well as providing sufficient oxygen for white blood cells to exercise their killing power.
The average mortality rate from intracranial abscess reported in six large studies was 20 percent when hyperbaric oxygen was not used. Among the 48 known cases treated with hyperbaric oxygen to date, the mortality rate has been only 2 percent. Additionally, most of the patients treated with hyperbaric oxygen have returned to their regular daily activity after recovery, with less apparent brain damage. Therapy with hyperbaric oxygen carries minimal risks.
Compromised Skin Grafts and Flaps
Skin grafts and compromised skin flaps represent a classical problem involving insufficient oxygen supply to tissue. Plastic surgeons use the grafts and flaps to repair serious damage, and to close or cover wounds. Skin is taken from one part of the patients, body and used to cover a break in the skin on another part. There are several types of skin grafts. They include full-thickness grafts, in which all of the skin layers are used, and split-thickness grafts, in which only the top layers and several of the deeper layers are used. There are also pedicle grafts, in which part of the skin remains attached to the donor site. This allows the old blood supply to remain intact while a new blood supply develops.
The problem is what to do when skin grafts appear not to be taking. A freshly applied split-thickness graft receives no oxygen until tiny blood vessels called capillaries can penetrate into it. Such capillary ingrowth normally takes place over a two to three day period. If this does not happen, it's not likely that the graft will survive. HBOT improves the chances that a graft will take, both by supplying oxygen and by encouraging quick capillary growth.
Providing hyperoxygenation increases the oxygen tension in the graft bed and wound margins up to 1500 percent. In turn, the hyperoxygenation causes a marked increase in the effectiveness of the blood or plasma that reaches the graft through compromised blood vessels. The volume of tissue that derives sufficient oxygen from a single damaged blood vessel increases 16 fold and marked tissue salvage results.
Lack of oxygen tends to be less of a problem with full-thickness and pedicle grafts since these grafts have their own supply of capillaries. Even so, it still takes time for good blood flow to become established through these type of grafts, Therefore, full-thickness and pedicle grafts also respond to HBOT. In the case of pedicle graft, it is important that HBOT be employed before what little circulation that is present develops blood clots.
In many instances HBOT is used only after a skin graft starts to fail. While HBOT can help save failing grafts it can be even more effective when used before surgery to keep grafts from failing in the first place.
HBOT also offers strategies for reducing edema. The edema reduction effect, induced by the relative spasm of a precapillary arteriolar sphincter helps to limit the swelling of the graft or flap. The high oxygen tension achievable with HBOT induces large oxygen neovascularization. Among other things, oxygen dissolved in plasma is readily available to tissues and organs thus limiting damage from reperfusion injury.
HBOT's effectiveness in aiding skin graft survival is supported by research. The effectiveness of HBOT is shown in grafting and in reimplantation of limbs, with a salvage rate of 75% for the HBOT group compared to 46% for the controls, with 100% HBOT salvage when the patient is treated within 72 hours post-operatively.
The use of HBOT for the preparation of a base for skin grafting and the preservation of compromised skin grafts has been well documented as effective.
Refractory osteomyelitis is a bone infection which has not responded to appropriate treatment. Hyperbaric oxygen increases the oxygen concentration in infected tissues including bone and kills or inhibits the growth of organisms which prefer low oxygen concentrations. These effects occur through the oxygen-induced production of toxic radicals or through an indirect effect medicated through the white blood cells (polymorphonuclear leukocytes).
Thermal burn injuries, if not fatal, can cause disastrous long-term physical and emotional disability for the survivor. Especially in closed space fires, thermal and smoke (products of combustion) damage to the lungs can occur requiring in some cases intubation and use of a mechanical ventilator.
Burn injuries characteristically progress to become deeper and more extensive with time. Peak damage occurs within 3-4 days after the initial burn, and can be up to 10 times worse than the initial burn injury. In more severe and/or extensive burns (deep second, third and fourth degree burns), multiple aggressive surgeries are generally necessary to excise the burned tissue and later to perform skin grafts to cover these areas.
Burn injuries can result in lifelong difficulties, physical limitations, loss of job and employment opportunities and significant disfigurement as the body heals from the injury. In many cases the burn victim's life is radically changed literally overnight and the psychiatric adjustments can be overwhelming. When possible, these injuries should be treated in centers that specialise in the management of thermal burns.
Adjunctive hyperbaric oxygen (HBO2) therapy has been shown to limit the progression of the burn injury, reduce swelling, reduce the need for surgery, diminish lung damage, shorten hospitalisation and result in significant overall cost savings. These benefits are more apparent if therapy is initiated within 6-24 hours of the burn injury.
Ideally, the patient should have 3 sessions in the first 24 hours, twice daily treatments until the process stabilizes, then continued therapy as indicated for healing enhancement and to support grafted areas. Indications for HBO2 therapy typically include deep second-degree and third-degree burns that involve greater than 20% of the total body surface area, and less extensive burns that involve the face, hands or groin area. Best results are realised when HBO2 is used as an integral part of an aggressive multidisciplinary approach to the management of this potentially fatal injury. HBO2 is a very safe therapy even in seriously injured patients when administered by those thoroughly trained in HBO2 therapy in the critical care setting and with appropriate monitoring precautions.