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Hyperbaric Oxygen Therapy

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Hyperbaric Oxygen Therapy also known as hyperbaric oxygen therapy (HBOT) is the medical use of oxygen at a higher than atmospheric pressure. Uses Certain non-healing ... – PowerPoint PPT presentation

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Title: Hyperbaric Oxygen Therapy


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
  • Decompression sickness
  • Air or gas embolism

3
Uses
  • 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
  • Decompression sickness
  • Air embolus syndrome

8
Secondary Effects
  • Vasoconstriction
  • Decreased inflow into tissues
  • Decreased edema
  • 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)
  • Toxin inhibition
  • Decreased clostridial alpha toxins (gas gangrene)
  • Decreased cardio toxins
  • Antibiotic synergy

10
Signs and Symptoms of Oxygen Toxicity
  • Nausea and vomiting
  • Dry cough
  • Seizures
  • Substernal chest pain
  • Sweating
  • Bronchitis
  • Pallor
  • Shortness of breath
  • Hiccups 
  • Muscle twitching
  • Pulmonary edema
  • Anxiety
  • Visual changes
  • Tinnitus 
  • Hallucinations 
  • Vertigo 
  • Decreased level of consciousness 

11
Contraindications
  • Claustrophobia
  • Pneumothorax
  • History of spontaneous pneumothorax
  • Chronic obstructive pulmonary disease
  • Seizure disorders
  • Upper respiratory infection
  • Hyperthermia
  • Malignant tumors
  • Acidosis
  • Anxiety
  • Gas Emboli/tension
  • Increased lung bleb
  • Increased risk seizures
  • Increased barotraumas

12
Organs Affected by Barotrauma
  • Sinuses
  • Middle ear
  • External ear
  • Inner ear
  • GI tract
  • 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. gt 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)
  • Thrombocytopenia
  • 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 lt 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.
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