Uses . Certain non-healing wounds (post-surgical or diabetic) Radiation soft tissue necrosis and radiation osteonecrosis Necrotizing fasciitis (flesh eating bacteria) Carbon monoxide poisoning Decompression sickness Air or gas embolism . Uses . Acute arterial ischemia (crush injury, compartmen
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1. Hyperbaric Oxygen Therapy
also known as hyperbaric oxygen therapy (HBOT) is the medical use of oxygen at a higher than atmospheric pressure.
2. Uses Certain non-healing wounds (post-surgical or diabetic)
Radiation soft tissue necrosis and radiation osteonecrosis
Necrotizing fasciitis (flesh eating bacteria)
Carbon monoxide poisoning
Air or gas embolism
Acute arterial ischemia (crush injury, compartment syndrome, etc.)
Compromised skin grafts or flaps
Severe infection by anaerobic bacteria (such as gas gangrene)
Severe uncorrected anemia when blood transfusion is not available (e.g., in a Jehovah's Witness)
Chronic refractory Osteomyelitis
4. HBOT and Medicare An HBOT session costs anywhere from $100 to $300 in private clinics, to over $1,000 in hospitals. More U.S. physicians are lawfully prescribing HBOT for "off label" conditions such as Lyme Disease and stroke. Such patients are treated in outpatient clinics, however it is unlikely that their medical insurance will pay for off label treatments.
5. Controversial HBOT is controversial and health policy regarding its uses is politically charged. Both sides of the controversy on the effectiveness of HBOT is available in the form of PUBMED and the Cochrane reviews, a discussion of Multiple Sclerosis in particular.
6. Mechanism and Effects Hyper-oxygenation Greater oxygen carrying capacity
Increased oxygen diffusion in tissue fluid
Diffusion distance proportional to the square root of dissolved oxygen
Severe blood loss anemia (unable to carry oxygen)
Crush injury, compartment syndrome graft, and flap salvage (decreased perfusion)
7. Mechanism and Effects
Edema (increased diffusion barrier)
Decrease gas bubble size
Boyle law - Gas volume inversely proportional to pressure
Hyperbaric diffusion gradient favors gas leaving the bubble and oxygen moving in, metabolizing oxygen in the bubble
Air embolus syndrome
8. Secondary Effects Vasoconstriction
Decreased inflow into tissues
Increased oxygen gradient between wound and surrounding environment
Increased fibroblast proliferation leading to increased collagen deposition and increased fibronectin, which aids in neovascularization
9. Additional Effects Leukocyte oxidative killing
Increased oxygen free radicals
Anaerobes lack superoxide dismutase to control oxygen free radicals (Necrotizing soft-tissue infections)
Decreased clostridial alpha toxins (gas gangrene)
Decreased cardio toxins
10. Signs and Symptoms of Oxygen Toxicity Nausea and vomiting
Substernal chest pain
Shortness of breath
Hiccups Muscle twitching
Decreased level of consciousness
11. Contraindications Claustrophobia
History of spontaneous pneumothorax
Chronic obstructive pulmonary disease
Upper respiratory infection
Increased lung bleb
Increased risk seizures
12. Organs Affected by Barotrauma Sinuses
Teeth Congestion and/or occlusion
Eustachian tube occluded Failure to equalize pressure within middle ear space
Wax build-up or ear plugs occlude canal
Oval or round window rupture
Gas in bowels, distention on ascent
Infected or restored teeth (may harbor gas)
13. Example Treatment Protocol Guidelines 2.0 ATA* oxygen X 90 min
2.0 ATA oxygen X 90 min with 10 min air break (high seizure risk)
2.5 ATA oxygen X 90 min
3.0 ATA oxygen X 90 min Wound healing compromised skin grafts and/or flaps Thermal burns Osteomyelitis Crush injury and/or compartment syndrome
MucormycosisWound healing Compromised skin graft and/or flaps Thermal burns Osteomyelitis Crush injury and/or compartment syndrome Mucormycosis
Nonclostridial gas gangrene Necrotizing infections Osteomyelitis (Escherichia coli or Pseudomonas species isolated) Late radiation tissue injury (osteoradionecrosis, soft tissue radionecrosis)
Carbon monoxide poisoning Clostridial gas gangrene
14. Oxygen content Oxygen Content = 1.34 mL of O2/g of Hb X g of Hb/100 cm3 X Percent Saturation
Above 200 mL of mercury of pressure, the oxygen dissolved in plasma significantly increases. This is calculated with the Henry law:
Dissolved Oxygen (vol %) = 0.0031 (mL O2/100 cm3/mm Hg) X PaO2
15. The total oxygen content of blood under hyperbaric conditions is equal to the oxygen content calculation plus the dissolved oxygen content. The average metabolic consumption of oxygen by the human body at sea level is 6.6 cm3/100 cm3 of blood. Under hyperbaric conditions of 3 atm while breathing 100% oxygen, the total dissolved oxygen content delivered is in excess of this metabolic requirement, meaning that oxygen can be supplied under these conditions even in the absence of hemoglobin.
16. Carbon dioxide, the byproduct of cellular respiration, is carried in the blood as bicarbonate (75%), as carboxy hemoglobin (20%), and dissolved in plasma (5%). Through the Haldane effect, the saturation of hemoglobin with carbon dioxide depends on deoxygenation. As oxygen is released from hemoglobin, carbon dioxide may combine. Under conditions in which the hemoglobin remains saturated, such as in hyperbaric medicine, the PaCO2 therefore may rise. Unless the normal respiratory compensatory conditions are present to exhale the extra carbon dioxide, the patient may develop significant carbon dioxide retention, as may be observed with chronic obstructive pulmonary disease.
17. Carbon monoxide poisoning Smoke inhalation injuries are common in house fires and other fire and/or smoke situations in closed spaces. Carbon monoxide, found in smoke, is the leading cause of poisoning deaths in the US. Carbon monoxide is a colorless, odorless, tasteless, and nonirritating gas that has a 210-fold greater affinity for hemoglobin than oxygen. Carboxyhemoglobin produces a leftward shift of the oxygen dissociation curve, making oxygen less available to the tissues (Haldane effect). The half-life of carboxyhemoglobin at room air, 100% oxygen, and 3 ATA 100% oxygen is 320, 90, and 23 minutes, respectively. This indicates HBO treatment for patients with carbon monoxide poisoning.
18. Carbon monoxide poisoning Indications for hyperbaric treatment of carbon monoxide poisoning include comatose patients, patients with ischemic changes on ECG, those with abnormal psychological and neurologic tests, those with carboxyhemoglobin levels greater than 40%, symptomatic pregnant patients or those with carboxyhemoglobin level greater than 15%, and patients who are symptomatic after 4 hours of 100% oxygen treatment.
19. Decompression sickness Naval investigations and experiments have increased understanding and treatment of severe decompression sickness ("bends"). During decompression or resurfacing, gases within the vasculature and other tissues come out of solution and expand to promote a mechanical and proinflammatory reaction. The gas bubbles disrupt vascular endothelium and nerve tissue, cause middle ear and cochlear dysfunction, foster edema via vascular and lymphatic occlusion, and promote ischemia by blocking vessels. Proinflammatory cytokines are released from neutrophils, platelets, and endothelial cells while the complement and coagulation cascade systems are activated. The CNS and other tissues develop microhemorrhages.
20. Decompression sickness Patients present clinically with joint and/or muscle pain, pruritus, edema, and mottled skin. More severe and ominous symptoms include upper lumbar cord and CNS dysfunction, cardia dysrhythmias, respiratory embarrassment, and severe abdominal pain. Onset of symptoms usually occurs within the first 30 minutes postdive but can take up to 12 hours. HBO attempts to reduce the bubble size until the inert gas is eliminated while tissues are hyperoxygenated.
21. Clostridial gas gangrene Clostridial gas gangrene is a life-threatening and/or limb-threatening infection that mandates emergent surgical intervention. Only use HBO in conjunction with surgery. Hyperbaric medicine works by a number of mechanisms to decrease the production of the alpha toxin released from clostridium, limit bacterial replication, and oxygenate tissues. Perform treatments immediately following surgery and continue them at least twice daily until evidence of the toxin hemolysis subsides.
22. Radiation injury Radiation injury alters the normal tissue physiology and anatomy. Marx observed the triad of hypocellularity, hypovascularity, and hypoxia in tissues subjected to radiotherapy. A progressive tissue fibrosis and capillary loss are associated with the endarteritis obliterans related to the sensitivity of cell lines (eg, endothelial cells, fibroblasts, muscle, nerve cells). The resulting tissue insult may manifest as nonhealing ulcers, pigmentary skin changes, tissue induration, loss of elasticity, and local erythema and tenderness. Bone may progress to an avascular necrosis. The central avascular region of ulcers and osteoradionecrosis is rendered hypoxic, and the surrounding tissues have greater oxygen content.
23. Radiation injury Hyperbaric treatment promotes angiogenesis and hyperoxygenation to the radiated affected tissues. Increasing the oxygen content to the surrounding tissues markedly increases the overall oxygen gradient between these tissues and the central hypoxic area. The increased oxygen gradient is the essential catalytic factor for angiogenesis. Multiple hyperbaric treatments are required to significantly increase the capillary density in the affected tissues. Prophylactic hyperbaric medicine is recommended by the National Cancer Institute for procedures (eg, tooth extraction) that are performed on irradiated mandibles.
24. Chronic nonhealing wounds Oxygen is required for angiogenesis (which is fostered by the increased oxygen gradient), collagen deposition, re-epithelialization, cellular respiration, and oxidative killing of bacteria. Decreased edema noted following hyperbaric treatment allows better diffusion of oxygen and nutrients through tissues while also relieving pressure on surrounding vessels and structures. In this light, HBO has been used for treating foot ulcers in patients with diabetes, venous and arterial insufficiencies, burn wounds, crush injuries, marginal flaps, and skin grafts. Before initiating hyperbaric treatment, optimize the patient's overall medical status, facilitate nursing care of the patient, and address local wound care and dressing.
25. Wounds with Diabetes Foot wounds of patients with diabetes offer a particularly difficult problem. These patients often have an impaired immune system, predisposing them to infections. Blood supply to the wounds is hindered by large and small disease. The red blood cells are sticky and nonpliable, which leads to capillary occlusion and distal ischemia. Neuropathies render the foot insensate and impair motor function. This impaired motor function flattens the foot so that the metatarsal heads become prominent and promote further susceptibility to ulceration via pressure.
26. Reperfusion injuries . These injuries result from the reperfusion that follows an extended period of ischemia. Oxygen free radicals rise, thromboxane A2 and adhesion molecules are activated, platelet aggregation occurs, and vascular vasoconstriction activity is increased. The endothelium is damaged, which promotes vascular leakage, edema, and thrombosis. Tissue necrosis ensues, and the activation of white blood cells is pivotal to the reperfusion injury. Using hyperbaric treatment that may increase oxygen free radicals to benefit the reperfusion injury seems paradoxical.
27. Effects of Pressure Patients inside the chamber will notice discomfort inside their ears as a pressure difference develops between their middle ear and the chamber atmosphere. This can be relieved by the Valsalva maneuver or by "jaw wiggling". As the pressure increases further, mist may form in the air inside the chamber and the air may become warm. When the patient speaks, the pitch of the voice may increase to the level that they sound like cartoon characters.
To reduce the pressure, a valve is opened to allow gas out of the chamber. As the pressure falls, the patients ears may "squeak" as the pressure inside the ear equalizes with the chamber. The temperature in the chamber will fall.
28. Inhaled Nitric Oxide Nitric oxide (NO) is a colorless, highly diffusible, and very toxic gas. It is also a promising new treatment in the battle against respiratory distress syndrome (RDS) and persistent pulmonary hypertension of the newborn (PPHN). Inhaled nitric oxide was first used on animals inflicted with pulmonary hypertension in 1991. Then in 1992, NO was used with some success in infants with PPHN . Although NO has been shown to be beneficial in some cases of RDS and PPHN, it is still considered to be an investigational drug by the FDA. All candidates for NO therapy must meet certain criteria passed down by the FDA.
29. NO is naturally formed within the vascular endothelial cells from L-arginine and molecular oxygen in a reaction catalyzed by NO synthase. The NO activates chemicals which lead to the relaxation of vascular smooth muscle. Scientists believe that NO production is impaired in the patient suffering from PPHN. Studies have shown that inhaled NO diffuses from the alveoli into smooth muscle causing relaxation. Thus proving that inhaled NO could be the potent pulmonary vasodilator that is needed.
30. Indications for inhaled Nitric Oxide Inhaled nitric oxide is indicated for the treatment of RDS and various other lung disorders characterized by pulmonary hypertension and hypoxemia. Other indications include pediatric patients with g.a. > 35 weeks through age 18 years that meet one or more of the following criteria:
Acute hypoxemic respiratory failure.
Documentation of pulmonary hypertension by a pediatric cardiologist as determined by right to left shunting and flattening or reverse curvature of the intraventricular septum
A 5-15 percent difference between pre- and postductal oxygen saturations
Informed consent by a parent
31. Contraindications for inhaled Nitric Oxide There are certain contraindications to the delivery of nitric oxide for the RDS patient and the infant with pulmonary hypertension. Some of the contraindications are:
Refractory hypotension despite adequate volume and vasopressor support
Lethal congenital anomaly
Life-threatening bleeding diathesis such as:
Intraventricular hemorrhage, grade III or higher
Active pulmonary or gastrointestinal hemorrhage
Disseminated intravascular coagulation (DIC)
Patients with a disease process that is refractory to any further medical support
32. DIC Disseminated intravascular coagulation (DIC)-The initial component of DIC is thrombosis of major blood vessels. The severity of the thrombosis depends upon the intensity of the precipitating disorder. Organs with larger blood flow are probably more affected than those with lower flow (skin, lungs, brain, kidneys). The second component of DIC is hemorrhage. Clot lysis with production of antifibrinolytic chemicals as well as depletion of clotting factors causes hemorrhage. The organ ischemia secondary to clot formation is the more lethal aspect of DIC causing multiple organ failure.
33. Thrombocytopenia Thrombocytopenia - an abnormally small number of platelets in the circulating blood.
Oxygen Index =FiO2 * MAP /PaO2
34. Equipment needed for delivery:
35. Normal Doses of Delivered Nitric Oxide: Most hospitals across the country start NO doses between 5-6ppm initially. The normal dose used throughout treatment is between 5-20ppm. If no response is recorded the dose may be increased gradually to a maximum dose of 80ppm. When the maximum dose is achieved and no response is noted then the patient is discontinued from this course of therapy and is considered a nonresponder to inhaled Nitric Oxide.
36. Complications of Inhaled Nitric Oxide: Nitric oxide in the presence of oxygen will in most instances combine to become nitrogen dioxide. Nitrogen dioxide can bring on respiratory distress even when delivered in low doses. The monitoring of NO/NO2 is very important for this reason. High levels of NO2 have produced pulmonary edema when extremely high doses of inhaled nitric oxide are used.
37. Another critical value to monitor is the formation of methemoglobin. Nitric oxide has been found to have an affinity for hemoglobin that is 280 times faster than carbon monoxide, therefore, continuous monitoring is essential. High levels of methemoglobin can potentially interfere with tissue oxygen delivery and result in hypoxia. At some hospitals, methemoglobin levels < 4% are considered acceptable. If at any time the level rises above that point then the concentration of inhaled NO should be reduced or discontinued completely.
38. Complications Methmoglobin (metHb) - a transformation product of oxyhemoglobin due to the oxidation of the normal Fe2+ to Fe3+, thus converting ferroprotoporphyrin to ferriprotoporphyrin.
39. Complications One other potential complication that should be mentioned is the possible effect on coagulation caused by decreased platelet aggregation. Although not fully understood, researchers do know that NO plays an important role in platelet aggregation and could have significant effects on coagulation.