Severe blood loss (anemia due to)

Average volume of blood in a healthy adult individual is some 5000 ml (3000 ml plasma + 2000 ml erythrocytes). After an episode of acute bleeding, an organism will compensate the loss of plasma within one to three days, but low red blood cell count will remain. In chronic blood loss that a patient cannot compensate, hemoglobin level is lowered to dangerously low values hence severe anemia exists. Lowered blood viscosity results in lowered resistance to blood flow through peripheral blood vessels that are dilated due to hypoxia. HBOT could temporarily meet the needs of an organism for oxygen even without blood and this is what makes this method a "bloodless transfusion". In cases of profound blood loss, when replacement of lost volume is not possible due to whatever reason, when problems of cross-matching exist, when there are concerns or doubts dealing with blood safety or due to religious beliefs, intermittent application of HBOT will enable enough oxygen for basic metabolic needs and normal functioning of all vital processes.

Ileus is a disease characterized by blockage of passage of intestinal content and gases through the intestinal tube. This is an urgent and life-threatening condition since it could, depending on mechanisms of onset and the speed of development, endanger the patient and cause death. There are two distinctive types; dynamic ileus that occurs due to paralysis of intestinal muscles, and mechanical ileus that occurs due to an obstruction of intestinal tube. Postoperative ileus or adynamic ileus occurs after surgery in the abdomen. It is a consequence of activation of spinal reflex by pain and intestinal inflammatory response. It is characterized by obstipation, severe abdominal pain, vomiting and fever. General status of the patient is very severe, dehydration often occurs, and abdomen is sensitive even to gentle palpation.

HBOT corrects hypoxia of the intestinal mucosa and prevents progression of damage as well as eventual perforation of the intestinal wall, recovery of motoric voiding of the intestinal tube and peristaltic of the small intestine.

• Crohn's disease is a chronic inflammatory disease characterized by inflammation that affects the entire tube of the digestive system. It could indeed affect any part of the digestive system, but the most common locations are terminal ileum and colon. Usual symptoms include chronic diarrhea, sometimes with traces of blood and mucus, spastic abdominal pain, increased body temperature, lack of appetite and loss of body weight. The cause has not been discovered yet, but it is assumed that some kind of autoimmune disorder is responsible for this condition. Inadequate or wrong treatment could result in complications such as fistulas, abscesses, strictures, obstructions and bleeding from colon. Therefore, the patients are forced to seek surgical help. Also, secondary inflammation of numerous other organs.
   
• Ulcerous colitis is a chronic inflammatory disease that exclusively affects colon. The changes are found on superficial parts of the mucosa and are most commonly localized on the left part of colon (sigmoid colon and rectum), however any part of colon could be affected and changes usually spread with the progression of disease to all parts of colon. Ulcers that cause diarrhea with traces of blood and mucus, increased body temperature and painful spasms, characterize inflammatory changes. Increased is morbidity from colon carcinoma in the patients who have the diseases longer than 10 years. In some of the patients, other autoimmune disturbances could also occur and complications other than on colon, such as iritis, uveitis, episcleritis, migratory polyarthritis, sacroileitis, erythema nodosum, thickening of  finger tips, etc.
   
• Pseudomembranous colitis is a disease that is most often, although not exclusively, caused by bacteria Clostridium difficile. Harmless intestinal bacteria maintain normal balance, preventing pathogenic bacteria from invading the intestine. However, many antibiotics that are taken orally will disturb the intestinal flora, allowing at the same time to Clostridium difficile to invade the intestinal tube and by releasing two toxins to cause strong inflammation of colon with pathological changes that are called pseudomembranes. The disease could be mild in nature but also escalate to a life threatening toxic colitis, with symptoms such as diarrhea, with or without blood, spastic pains in the abdomen and increased body temperature. In severe form of the disease, dehydration, toxic megacolon, shock will occur. The most severe forms of the disease will have fatal outcome.

In intestinal inflammatory diseases, HBOT lessens pain, lessens inflammatory reaction, lowers number of stools, diminishes quantity of blood and mucus, lessens edema of the intestinal wall, enhances healing of damaged mucosa, induces Crohn's disease into periods of long remissions and stable course, heals ulcerous colitis, lessens need for surgical interventions or delays them, and ameliorates immune status of patients.

Glaucoma is a chronic progressive disease that is manifested by an increase of intraocular pressure, damage to the head of the optic nerve and damage to the visual filed. It is caused by a blockade in the trabecular system where chamber fluid is drained from the eye. Since those microscopically routes are blocked, intraocular pressure develops causing slow but progressive loss of vision. Peripheral vision is first affected. Postponing of the treatment will gradually result in complete loss of vision. In some patients with glaucoma, blind spots in visual field will remain even after the pressure is normalized, and in some patients blind spots will occur even if no increase of intraocular pressure is detected (low pressure glaucoma). This supports the theory in accordance which disturbances of microcirculation in the head of the optic nerve and in the posterior segment lead to the loss of vision. Diagnosis is established by measurements of intraocular pressure and visual field. The goal of the treatment is to open uveo-scleral routes and protection of retina ganglionic cells.

HBOT increases and stabilizes visual field. Damaged peripheral vision and visual field defects (blind spots) recover. It would be ideal to provide two HBOT series per year to achieve the best results.

Brain edema often develops as a part of many diseases of the central nervous system. Generalized edema is a process that vitally endangers patient due to increased intracranial pressure. Conventional treatment of brain edema and increased intracranial pressure includes the usage of steroids, osmotic diuretics, by induction of barbiturate coma and by drainage of brain chambers.

HBOT lessens brain edema by lessening blood flow during vasoconstriction, with preservation of brain oxygenation, compensates the effect of ischemia and hypoxia caused by brain edema and breaks the vicious circle of events such as hypoxia/edema and further brain tissue deterioration.

Cerebral insult (insult, weakness, cerebral palsy) is a sudden neurological deficit caused by disturbance of brain blood flow. The term includes both ischemic and hemorrhagic incident. Ischemic cerebral insult happens when a blood clot or embolus blocks or slows down blood flow in the brain artery, thus blocking transport of oxygen and glucose that are necessary for regular function of the brain. It could be also caused by a spasm of brain arteries, without any obstruction of the arterial flow. In the brain tissue that has remained without oxygen necrotic damage or infarction occurs, with consecutive peripheral motoric and sensory defects. Hemorrhagic form is caused by bleeding and is therefore also called cerebral hemorrhage, mainly due to the rupture of brain aneurism or weakened or inflamed brain vessel. Bleeding causes an increase in intracranial pressure that damages tissues and cells. This type of brain insult has a mortality of some 80%.

HBOT lessens brain ischemia and hypoxia, facilitates oxygen delivery to tissues by lower blood viscosity, lowered aggregation of thrombocytes and increased elasticity of erythrocytes, lessens edema of brain tissue affected by infarction, lessens edema of cells ameliorating their metabolism, enhances oxygenation of cells in the zone of ischemic shade (ischemic penumbra; the zone between the zone of infarction and vital tissue containing cells in danger but alive and could be saved), prevents glycolysis and consecutive lactic acidosis and maintains metabolic functions of the jeopardized brain zone.

Brain injury (post-traumatic encephalopathy):
The treatment of brain injuries is focused on the cascade of events that occur after an injury: ischemia and tissue edema, an increase of intracranial pressure, destruction of cells and metabolic and enzymatic disturbances. The efficiency of the treatment is based on the possibility of brain tissue recovery. HBOT, together with other non-surgical options, should be considered as an adjunct to surgical intervention or as a primary option if surgery could not or will not be performed for whatever reason.
HBOT causes vasoconstriction thus diminishing blood flow through the brain and consecutively diminishes edema, whilst enhanced oxygenation suppresses ischemia and consecutive neural tissue damage. Lower blood flow lowers the influence of increased blood pressure. It has been demonstrated that HBOT per se lowers increased intracranial pressure.

Spinal cord injury:
Key goals of application of HBOT in the treatment of spinal cord injury are lessening of edema and correction of ischemia. The development of spinal cord injury includes ischemia of gray matter and increased blood flow in spinal cord with edema of white matter. Consecutively, loss of function and paralysis below the level of injury occur.
If HBOT is applied in the treatment, some neural tissue damage caused by hemorrhage, not by shearing, is reversible. HBOT lessens ischemia in the gray matter, lessens edema in the white matter and corrects biochemical disturbances at the site of spinal cord injury. Rehabilitation is the most important part of the entire therapy of a spinal cord injury patient. HBOT increases capacity for physical exercise in patients with neurologic deficits, lessens metabolic complications of tiredness, increases lung vital capacity and lessens muscular spasticity.

Vascular headaches include migraine (with or without aura) and cluster-headaches.

• Migraine is a term used to define a group of severe usually unilateral repetitive headaches, accompanied by nausea, photofobia, sonophobia and vomiting. Some 30%-40% of all migraine attacks start with an aura, with transient neurological defects, that appear some 20 minutes before the actual headache attack. It is considered that aura is connected with focal reduction of circulation in the brain that is probably caused by arterial vasoconstriction followed by vasodilation and pain. Aura could be manifested as flashing or zigzag lights, lines and dots, blurred vision, facial or arm twitches, weakness in arms and/or legs, speaking disturbances and confusion.
   
• Cluster-headaches mainly occur in men. Clinical picture includes strong, unilateral, retro-orbital pain accompanied by tearing in one eye, lowered eyelid, changes of pupil and stuffy nose. The patients suffer attacks of severe headache on one side of the head lasting for about one hour, one to three times a day. The headaches often occur at the same time of the day, what gives the name cluster. The headaches occur during several weeks or months, but could vanish for several months or years, only to reappear.

HBOT causes an increase of oxygen in blood to the levels much higher than under normal pressure. The ability of vasoconstriction of painfully dilated blood vessels is much higher, representing protective reaction of blood vessel walls against increased blood oxygen. Cerebral edema and pain are ameliorated due to lower blood flow and better oxygenation.

Regardless of all usual measures, diet, exercise, surgical care and drug therapy, all complications of diabetic disease are an indication for HBOT. However, HBOT also plays an important role in the prevention of complications.

• "Diabetic foot" (please, check the part about chronic wounds)
• Arterial insufficiency I. - IV. degree and diabetic angiopathy: HBOT induces anti-oxidative defense mechanisms important for slowing down the atherosclerotic process and for correction of the existing atherosclerotic changes, and stimulates neoangiogenesis.
• Diabetic polineuropathy: HBOT enhances motoric functions of peripheral nerves and recovery of peripheral sensitivity.
• Diabetic retinopathy and maculopathy: HBOT lessens or changes the need for laser photocoagulation that leaves permanent scars on retina.

Diabetic retinopathy is an often complication of diabetic diseases, characterized by changes on small blood vessels of the eye retina. High blood sugar values cause damage to small blood vessels in the eye retina in sense of thickening of basal membrane and an increase in permeability of retinal blood vessels (non-proliferative phase, with no changes of visual acuity). In some patients, macular edema would develop due to leakage of liquid and lipids to retina through damaged blood vessels, with partially blurred vision. With the progress of the disease, diabetic retinopathy reaches the advanced stage or proliferative phase that occurs due to the lack of oxygen in retina and is manifested by formation of new, fragile blood vessels all over retina. If no early treatment is applied, bleeding occurs, blurred vision and finally blindness. Fibrovascular proliferation could cause retinal ablation. Also, blood vessels could grow in to the corner of anterior eye chamber, with consecutive neovascular glaucoma. Diabetic retinopathy occurs in almost 80% of all the patients suffering from the diabetic disease for 10 years and longer.

HBOT stops retinal bleeding, enhances vision, also lessens or changes the need for laser photo-coagulation that leaves permanent scars on retina.

Mb. Raynaud is a disease of blood vessels of unknown origin. It is manifested as spasms of small arteries, most commonly of fingers and toes, sometimes on other parts of the body (nose, ear, tongue). The main symptom is intermittent paleness and cyanosis, sometimes also pain. In 60 to 90% of the cases, the patients are young women, already suffering from sclerodermia, although the disease could be the only one.

HBOT lessens pain, enhances microcirculation and oxygen delivery to the affected limbs, as well as stimulates growth of new blood vessels.

Mb. Burger is a disease of small and middle size arteries and veins of extremities. It is most common in male smokers. The leading symptom is pain in arms and legs, cyanosis and feeling of cold in fingers and toes. In more severe cases, necrosis and gangrene are a complication.

HBOT increases partial pressure of oxygen in ischemic/hypoxic tissues, lessens tissue damage and necrosis and the size of pathological changes, stimulates wound healing and lessens pain. In case of gangrenous changes, enhances formation of demarcation line between dead and vital tissue, thus helps defining a decision about the level of an amputation.

• Crush injury is a severe injury of two or more tissues (muscles, bones, other connective tissues, skin, nerves) that jeopardizes their survival due to its extensiveness. Consecutive edema and damage to blood vessels increases lack of oxygen and leads to irreparable tissue damage and loss of function. Under hypoxic conditions, the tissues lose ability to fight infection and recovery from injury is also jeopardized. The basis of the treatment is wound and fracture care, antibiotic treatment and surgical measures as indicated. Numerous data suggest the necessity of early application of HBOT into the arsenal of therapeutic weapons. If HBOT is postponed for 5 or 6 hours and if at the same time the affected limb is bluish and swollen, limb survival prognosis gets worse. HBOT lessens tissue hypoxia by increasing partial pressure of oxygen, lessens edema, enables survival of endangered tissues, promotes wound healing, prevents infection and lessens effects of reperfusion injury.

• Compartment syndrome occurs when pressure of fluid inside muscular compartment of an extremity becomes higher than the pressure within capillary network, thus leading to ischemia, loss of function and tissue necrosis. Standard surgical intervention in such cases is fasciotomy (muscular fascia is cut to relieve tension).

HBOT is applied to prevent further damage to the affected tissue, however HBOT should not be understood as a replacement for surgical decompression. HBOT could prevent further deterioration until surgical measures are finally undertaken. After surgical decompression, if neurological damage or muscular necrosis still persists, HBOT could increase chances for survival of vital tissues on the rim of the damage.

Bell's palsy or paralysis is also called idiopathic facial paralysis. This entity does not include facial paralyses of other origin, such as after trauma, tumor or after surgery. Its cause is unknown. It could occur due to microcirculatory disturbances that lead to edema of facial nerve within the bone canal the nerve goes through. As a consequence, that causes increased pressure affecting the nerve, insufficient blood supply and paresis. This palsy heals spontaneously in some 80% of all cases, but in many cases it takes months of uncertainty before any result would occur.
 

Standard therapy includes steroids, blockage of facial nerve, vitamins and physiotherapy. Surgical method in the treatment of Bell's palsy is aimed to decompress the nerve from the bone canal. Mild or more severe residua would be apparent in some 20 or 30% of all cases, even after a prolonged treatment.

HBOT corrects hypoxia, lessens tissue edema thus leading to decompression of facial nerve in the bone canal, and maintains necessary oxygenation level until the termination of the pathological process. HBOT is always recommended with physiotherapy, since the percentage of the cured after such therapeutic approach is greater. The treatment should be commenced as soon as possible, but the best results are achieved if HBOT is started within 7 to 10 days.

Sudden loss of vision most commonly occurs as a consequence of obstruction of central retinal artery, that is usually a part of atherosclerotic or inflammatory arterial disease, but also due to other disturbances. The most common symptom is sudden and painless unilateral blindness caused by a clot from atherosclerotic plaque of the carotid artery on the same side. Although blindness develops within seconds, retina cells are relatively resistant to hypoxia and could survive even up to 22 minutes after blockage of circulation. Standard treatment includes paracentesis of front eye chamber, retrobulbar blockade with an anesthetic, anticoagulant drugs, etc. However, none of the treatments have been found satisfactorily beneficial.

Combined with standard therapy, HBOT is efficient in correcting damage due to thrombosis of central retinal artery as well as in lessening edema due to thrombosis of central retinal vein. If applied immediately or within a couple of hours after the occurrence of blindness, HBOT will lead to full vision recovery in almost all cases.

Sudden deafness is hearing damage that occurs suddenly within several hours or days. The cause of sudden hearing loss is most often difficult if not impossible to establish. It could happen after a viral infection, but also due to vascular changes, autoimmune disease or the cause could remain unrevealed. None of the existing theories has been univocally accepted. The damage most often occurs unilaterally, and is manifested as sudden hearing loss in one ear, feeling of fullness and blockage, and often there is tinnitus accompanied by vertigo. Hearing loss is established by audiometric exam and analysis of tonal audiogram. Standard treatment includes vasodilators, steroids and vitamins, but with very different success.

Tinnitus (ringing ears) is the most common symptom of inner ear damage. It occurs as a consequence of acute acoustic injury, hypotension, after usage of ototoxic drugs, after stress and viral infections. It could be acute or chronic, and the treatment is mainly symptomatic.
HBOT increases partial pressure of oxygen in inner ear, ameliorates microcirculation and rheological properties of blood, lowers hematocrit and thus blood viscosity, and increases erythrocyte elasticity.
It is important to commence with HBOT as soon as possible after the occurrence of problems.

Subacute and chronic arterial insufficiency is a term used to describe all conditions with narrowed or blocked parts of arteries that supply limbs with blood. Lower limbs are more often affected. The most common symptom is pain in the affected limb. When legs are concerned, pain appears in calves after a few tens of meters of walk (claudication), and disappears at rest. Pain at rest is a sign of a severely advanced disease and arterial narrowing. Besides surgical measures and drugs, HBOT plays an important role in the treatment of arterial insufficiency and in the prevention of spreading of the disease. HBOT induces anti-oxidative defense mechanisms responsible for slowing down the atherosclerotic process and for correction of the existing atherosclerotic changes, increases partial pressure of oxygen in ischemic/hypoxic zones, lessens pain and influences walking distance in the patients with intermittent claudication.

HBOT is widely used to treat chronic wounds and ulcers caused by arterial insufficiency, as well as diabetic, venous, decubital, trophic and neuropathic ulcers.

• Diabetic ulcers usually affect feet, hence the name "diabetic foot". Pathological process on arteries persists even in patients with well-controlled glycaemia. As a result of that process, occlusive disease of large blood vessels and pathological changes on small blood vessels could develop. Additional problems include diabetic neuropathy and secondary wound infections. Standard treatment of the diabetic foot includes control of blood sugar, representative wound care and prevention and treatment of infection.
  It has been well established that HBOT lessens number of amputations, necessity for insulin, and fights hypoxia and infection.

• Venous ulcers are one of manifestations of chronic wound insufficiency, which is defined as hypertension in superficial or deep veins of lower limbs. Trophic changes that lead to venous ulcers are caused by ischemia in microcirculation and by edema that exists due to increased capillary permeability and slow lymphatic drainage. The treatment of venous ulcers includes elevated position of the limb, compressive therapy, and careful wound dressing as well as local therapy of ulcers and surgical measures. HBOT stimulates healing of venous ulcers.
   
• Decubital or trophic ulcers occur due to pressure on skin that oppresses circulation in the area of contact. Such ulcers would occur after long immobility in one position. Usually could be found in sites with bone prominences, such as heel and sacrum. Ulcer is a consequence of damage of ischemic skin, bacterial invasion and infection.
  HBOT lessens inflammatory reaction, stimulates granulation and epithelization.

• Ischemic ulcers develop as a consequence of insufficient peripheral arterial circulation caused by various diseases. They are mainly found on feet and/or hands. Primary treatment of persistent ischemic wounds on lower limbs is surgical revascularization and adequate wound care.
  HBOT has manifested positive effects in cases when the wounds would not heal despite maximal previous surgical revascularization or when revascularization was not possible. HBOT enhances healing or helps preparing vascular bed for skin transplant.

Effects of HBOT in the treatment of chronic wounds:

• Stimulates activity of fibroblasts and deposition of collagen necessary in the wound healing process;
• Corrects tissue hypoxia, stopping vicious circle of hypoxia and enables better and faster wound healing;
• Stimulates neoangiogenesis in compromised circulation, especially in acute traumatic ischemia;
• Enables bactericidal and bacteriostatic oxygen effect in infected wounds;
• Lessens pain and edema in the surrounding tissue.

After radiotherapy (treatment by radiation), some damage of a certain level to healthy tissues would usually remain in the exposed field. Even when protocols with low doses are used, one of possible complications is radiation tissue necrosis. Damage progresses slowly and long after the therapy has stopped. In the exposed tissue, due to lack of oxygen, collagen is lost and fibrosis increases, atrophy of skin and wounds appear, as well as osteoporosis. HBOT stimulates neoangiogenesis (formation of new blood vessels), thus microcirculation is enhanced, immune response is better, wounds cure faster, production of collagen is stimulated, lessens the depth of injury, protects vital marginal tissue and enhances epithelization.  Cost of treatment and rehabilitation are lower. The percentage of successfully treated is very high.

Covering of open wounds with skin is accomplished by transposition of skin in the form of a graft or flap, or skin transplantation in full or partial thickness. Certain risk always exists since such a procedure is inevitably characterized by insufficient supply of the transplanted tissue with blood and/or oxygen. Therefore, the procedure will fail in certain number of cases.

HBOT enhances damage to the transplanted tissue caused by lower concentration of oxygen (hypoxia/ischemia), ameliorates microcirculation and lowers thrombocyte aggregation, increases number and size of blood vessels in microcirculation (ideal preparation of surgical site), fastens production of healthy granulation tissue, stimulates activity of fibroblasts and synthesis of collagen.

• Burn is thermal injury that causes damage and necrosis of skin and subcutaneous tissue. The depth and severity of damage depends on strength of heat source and time of exposure. Tissue damage includes also blood cells damage that results in edema and inflammatory reaction.
   
• Frostbite injury is local and acute damage of skin and subcutaneous tissue caused by a prolonged exposure to extreme cold. Most commonly affected are peripheral body parts, such as nose, ears, fingers and toes. Initial skin changes are manifested as induration of skin, pale color, later reddish and bluish skin. Affected area is usually less sensitive although a strong pain could also be present. Sudden cease of sensation of cold is a reliable sign that the cold injury process has begun. Reversible at the beginning, damage soon becomes irreversible. Frostbite injury could be either superficial or deep. In case of superficial injuries, boils filled with clear liquid appear after a couple of hours but even days. Deep injuries affect subcutaneous tissue, sometimes muscles, tendons and bones. Boils filled with liquid with traces of blood or appear on the surface. Untreated frostbite injury mainly ends as infection and gangrene.

HBOT lessens edema and inflammatory reaction, prevents wound infection, stimulates epithelization and regeneration of skin, lessens the depth of injury and loss of fluid via damaged tissue. In case of corrective surgical attempts, HBOT enhances survival of skin grafts, corrects lack of oxygen in tissues, hospital stay is shorter and necessity for later surgery.

Mb. Sudeck is also known as "the complex pain syndrome" affecting usually limbs, almost exclusively in the adults. Etiology and pathogenesis are poorly understood. Most often, the trigger is an injury or a surgery with prolonged immobilization. The symptoms are manifested in three degrees, from inflammation and pain in the affected limb during rest and exercise, edema and sweating, to first stiffness of joints with muscular deterioration, cold, bluish skin and x-rays findings of diffuse patchy osteoporosis. The treatment includes pain therapy, physiotherapy and HBOT. HBOT causes local vasoconstriction, lessening edema and pain, ameliorates microcirculation and oxygen supply to soft tissues and bones of the affected limb.

Dysbaric osteonecrosis is a term used to describe aseptic or avascular bone necrosis due to ischemia caused by gas bubbles, although the exact mechanism is still a matter of controversy. Typically it is a disease of deep-sea professional divers but affects more often recreational divers as well. Most commonly are affected long bones of arm and leg. The symptoms develop after a delay lasting from several months to several years after decompression. Diaphyseal damages are painless. Pain and disability are related to the damage of joints. Possible are fracture and deterioration of head of humerus or femur. There has been no satisfactory conservative treatment so far. Surgical treatment is aimed to removal of necrotic bone, bone transplantation or joint immobilization. The best prevention of dysbaric osteonecrosis is recompression therapy in all cases of decompression sickness.

HBOT is usually provided in long series of up to 120 exposures, if not even longer. HBOT increases partial pressure of oxygen in tissues, thus preventing further deterioration of bone cells, causes vasoconstriction, thus lessening edema and enhances perfusion, stimulates neoangiogenesis, osteogenesis and lessens pain.

Gas gangrene is an acute, painful, necrotizing infection of soft tissues. It can develop after a trauma, after wounds caused by high velocity projectiles, complicated fractures, deep infected wounds, incorrectly performed abortions, and various surgical interventions. It is a consequence of infection by anaerobic, clostridial bacteria that form gas and exotoxins thus leading to tissue edema with consecutive loss of blood flow, oxygen pressure and leukocyte count, which leads to spreading of infection.

Gas gangrene treatment is based on intensive care, high doses of antibiotics, surgical measures and HBOT. HBOT inhibits toxin production, corrects hypoxia, causes significantly better oxygenation in vital tissue and in the tissue in the vicinity of infected area, and enhances antibiotic activity and immune response as well.

Aseptic bone necrosis is a disturbance of bone vascularization that leads to damage and loss of bone structure. Clinically it is manifested as pain and loss of function of the affected joint. There are several reasons for this condition, but in many cases an injury is considered to be the cause of the problem. Besides, the cause could also be gas embolism of bone blood vessels, thrombosis, fat embolism or arterial stenosis. Cellular damage leads to edema and inflammatory response of tissue, with consecutive pain and limited excursions of a joint that are also the leading symptoms of this disease. The most commonly affected are long bones of arm and leg. X-rays and often magnetic resonance of the affected bone are used in the diagnostic process.

HBOT increases partial pressure of oxygen, thus halts further deterioration of bone cells, causes vasoconstriction, lessons edema and enhances perfusion, stimulates neoangiogenesis and osteogenesis, and diminishes pain. The treatment is a long-term but effective. Ameliorating of symptoms is not a hallmark in evaluation of therapeutic success. A confirmation of increased bone density is needed to evaluate the healing process.

Osteomyelitis is an inflammation of bone tissue caused by an infective agent. Infection of a bone could occur after fracture or if an infectious focus in the very proximity of a bone exists (infection from the outside or exogenous infection) or could enter a bone by blood (hematogenous infection, infection from the inside or endogenous infection). In the affected bone tissue apparent are ischemia and hypoxia. Clinical picture could be manifested as acute, subacute or chronic.

Chronic osteomyelitis is an infection of bone lasting longer than 6 months with all histologic and radiologic signs of an infection or positive microbiological culture of bone fragment. The term "refractory" refers to the cases in which the defect would not heal despite all the measures, including surgical measures and antibiotic treatment. In the treatment of osteomyelitis, standard treatment includes surgical measures, antibiotics and HBOT.

HBOT will enable repair of bone tissue and an increase of partial pressure of oxygen from hypoxic to normoxic or even hyperoxic level, that results in stimulation of new blood vessels growth, increased production of leukocytes and their activity in the affected zone, enhanced transport of aminoglycosides over bacterial membrane, stimulated bone turn-over, i.e. osteoclastic (removal of necrotic bone tissue) and osteoblastic activity (growth of new bone tissue).

Numerous infectious organisms could cause brain abscess, amongst them the most often are anaerobes. Due to its structure, lack of vascular network and oxygen, abscess is difficult to treat with antibiotics that are otherwise first therapeutic option. Surgical drainage is used in encapsulated abscesses that would not heal or cause increase of intracranial pressure. Morbidity due to cerebral abscess is high, and there are severe neurological residua in the survived. In complicated case, when surgical treatment is not an option, HBOT is recommended, especially due to the fact that the causing bacteria are mainly anaerobic. HBOT lessens brain edema, has bactericidal effect, act synergistically with antibiotics and enhances defense mechanisms of organism.

Infection is an invasion and growth of a biological agent (microorganism) in the body of a host. Microorganisms are viruses, bacteria, parasites and fungi. Infection compromises normal functioning of host organism that could lead to the development of non-healing chronic wounds, tissue necrosis, extremity loss, even death. Inflammation is one of reactions of our organism against infection. The first and the most important defense line are leukocytes. Partial pressure of oxygen and quantity of oxygen play an important role since oxygen acts as an antibiotic interfering with bacteria metabolism. This effect is not selective but is present in a broad spectrum of microorganisms. The most efficient effect is seen in anaerobic organisms.

Application of HBOT:

• Enhances phagocytosis that is compromised in hypoxia;
• Increases partial pressure of oxygen in tissues and enables adequate oxygen supply to the infected area;
• Produces free oxygen radicals that are toxic for bacteria;
• Enhances wound healing;
• In bone infections, helps removing necrotic bone (osteoclastic function) and speeds up new bone formation (osteoblastic function);
• Stimulates immune mechanisms,
• Combined with sulphonamides, acts synergistically and increases their effect 5 to 10 times;
• Efficiency in the treatment of infections resistant to other drugs;
• Potentiates effect of aminoglycosides;
• Exerts bacteriostatic and bactericidal effects;
• Halts production of egzotoxin, namely α-toxin produced by Cl. perfringens, and detoxifies some toxins, namely θ-toxin produced by Cl. perfringens.

HBOT could be used as an adjunct in the treatment of fungal infections, especially with Candida albicans and in Rhinocerebral mucormycosis. Rhinocerebral mucormycosis is a fungal infection of lungs, brain, intestine and bones (maxillary, orbital and temporal), that most often occur in immunocompromised.

HBOT is a valuable adjunct to surgical and antibiotic therapy in necrosis and infections caused by aerobic or anaerobic bacteria. Such conditions include necrotizing cellulitis, progressive dermal gangrene, anaerobic streptococcal myositis and many others. Increase of partial pressure of oxygen in tissues has a strong effect on wound healing dynamics. This effect is mediated by an increase in leukocytes count, bactericidal activity and stimulation of production of collagen and fibroblastic activity necessary for the growth of new blood vessels.

Decompression sickness is a disease of divers and workers who breathe air at an increased pressure. It is caused by inert gas bubbles in tissues, most commonly nitrogen bubbles, mainly due to inappropriately fast ascent. The disease occurs in two main forms: type I., is considered to be a more mild form, affecting skin, muscles, bones and joints, while type II. is usually considered to be a more severe form, affecting all other organs (brain, spinal cord, heart, lungs, digestive system).

The only correct treatment is urgent decompression and HBOT until all symptoms disappear. This treatment modality will eliminate gas bubbles from the tissues and by ventilation via lungs. Breathing 100% oxygen corrects damage that affects nervous and other tissues due to hypoxia, corrects edema and reestablishes normal tissues and organs functions.

The most common source of CO poisoning are exhaust gases of automobile engines, heating systems, fumes from faulty chimneys and fumes from industrial sources. CO blocks transport, availability and utilization of oxygen in the body due to its extremely high affinity for hemoglobin, which is the principal carrier of oxygen to various tissues and organs. As a consequence, damage to the tissues occurs, mainly in the tissues with high oxygen demand, such as brain and heart.

HBOT hastens elimination of CO from blood, hastens recovery of neurological symptoms and lessens brain edema. If applied at an early stage of poisoning, HBOT lowers incidence of late neurological consequences. HBOT is also used to treat late consequences of CO poisoning. It is important to refer the patient with signs and symptoms of poisoning to hyperbaric medicine facility as soon as possible.

Gas embolism is a condition caused by entry of air into arterial or venous circulation. It mainly occurs as a consequence of an invasive medical or surgical procedure. It is also possible in divers usually after rapid ascent (pulmonary barotrauma). Clinical symptoms are mainly neurological or cardiological and depend on patient's position, way of air entry and gas volume, bubble size and speed of entry of gas into circulation. Regardless of mechanism of onset, HBOT is always a treatment of choice.

HBOT diminishes gas bubbles' size, causes bubbles to disappear from circulation, lessens edema of affected tissues, high partial pressure of oxygen ameliorates consequences of lack of oxygen in tissues with insufficient blood supply, recovery of damaged but alive cells in ischemic penumbra (shade).