An introduction to hyperbaric oxygen therapy for the ET nurse

WOUND CARE SECTION EDITOR: Barbara Bates-Jensen, MN, RN, CETN

An Introduct on tO Hyperbar c Oxygen Therapy for the ET Nurse M a r y W. Surman, RN, BSN, CNOR, CHT, CETN

yperbaric oxygen therapy, a controversial field of medicine that is not yet well understood, is the use of pressurization to deliver increased oxygen concentrations to the body a n d in particular to increase the amount of oxygen diffused in the p l a s m a . This article is intended to provide ET nurses with a n introduction to the physics of hyperbaric oxygen therapy and to illustrate how this therapy m a y be beneficial in aiding healing in selected patients. Methods of oxygen delivery, a review of the physics of hyperbaric oxygen therapy, including a brief explanation of the gas laws pertinent to hyperbaric oxygen therapy, and clinical considerations (clinical effects, implications, indications, contraindications, assessment parameters, treatment protocols, risks, side effects, a n d wound dressings suitable for this specialized environment) are discussed. Approved indications for hyperbaric oxygen therapy a n d contact information for locating the nearest hyperbaric oxygen therapy facility are included. (J WOCN 1996;23:80-9 I)

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Ms. Surman is currently employed as an ETnurse at Our Lady of the Lake Regional Medical Center, Baton Rouge, Louisiana. She was. graduated September 1994from the Emory University Wound, Ostomy and Continence Nurses Education Program. Thisarticle was submifled in consideration for the Gladys Frey Student Man uscript A ward. Reprint requests: Mary W. Surman, RN, BSN,CNOR, CHT, CETN, Our Lady of the Lake Regional Medical Center, ETDepartment, Clinical Enterprises, 7000Hennessy Blvd., Baton Rouge, LA 70808. Copyright © 1996by the Wound, Ostomy and Continence Nurses Society. 1071-5754/96 $5.00+ 0

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Hyperbaric oxygen therapy (HBOT) is the use of pressurization to deliver increased oxygen concentrations to the body and in particular to increase the amount of oxygen diffused in the plasma. Hyperbaric therapy has a long and diverse past, with the first use of a hyperbaric environment by Henshaw in the 1600s.I Henshaw used a large pair of organ bellows to compress (pressurize) an airtight room (domicilium) "to help digestion, to promote insensible respiration, to facilitate breathing and expectoration, and consequently, of excellent use for the prevention of most afflictions of the lungs."' Hyperbarics then died out until the 1800s. In 1834, a French physician,

Junod, used hyperbarics to treat lung ailments. In 1860, the first chamber in North America was opened in Canada, and in 1861 Corning opened the first chamber in the United States. Fontaine has been credited with the development of a mobile hyperbaric Operating theater in 1877. Cunningham opened the largest of all hyperbaric chambers in 1928 in Cleveland. Cunningham received several requests from the American Medical Association for documentation of claims of the effectiveness of hyperbaric treatments, and the chamber was forced to close after Cunningham refused to reply to these requests.' Unlike these early chambers, which used compressed air for their treatments, hyperbaric therapy with compressed oxygen was first used early in the century to manage the bends, also known as decompression illness. In the Netherlands during the 1950s, Ite Boerema used hyperbaric chambers and compressed oxygen to perform heart operations. Boerema and associates' landmark study, "Life Without Blood, "2 was published in 1960 and demonstrated the effectiveness of hyperoxygenation of the plasma in supporting life in the absence of hemoglobin. The physiologic effects of hyperoxygenated plasma account for the therapeutic results provided by HBOT. HBOT has long been accepted as the treatment of choice for the bends, which can occur in scuba divers who surface too rapidly. It can also be used to help victims overcome by carbon monoxide to recover with little or no neurologic deficit. In addition, HBOT is relevant for the ET nurse because it has been approved for treatment of selected nonhealing wounds and compromised skin grafts and flaps.

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METHODS OF DELIVERY HBOT can be delivered in several ways. With the first method of delivery, the patient is placed lying down in a monoplace chamber, an acrylic single-person device that is filled with 100% oxygen and pressurized (Figure 1). The patient then breathes the oxygen without the use of a mask or hood. Monoplace chambers are equipped with a two-way intercom system so that the nurse or technician can communicate with the patient throughout the treatment. A second method of delivery is to place the patient and a trained technician or nurse in a specially constructed room that is then pressurized with compressed air. The multiplace chamber is a free-standing metal cylinder that has been described as resembling a submarine (Figure 2). In a multiplace chamber, the patient breathes the oxygen through a hood or mask (Figure 3). T-tubes and neck collars may be used on patients with tracheostomies. These chambers can be configured to hold from two to 18 people, including a nurse or technician who stays with the patients during their treatment. The advantage of the multiplace environment is twofold: (1) a nurse or technician can provide "hands on" care of the patient and (2) the chamber is pressurized with air as opposed to oxygen, and this presents less of a fire hazard. Most hospital-based HBOT chambers are equipped to accommodate critical care patients by providing monitoring of arterial pressure, central line pressure, and electrocardiomyography. Special ventilators are available for patients requiring mechanical ventilation. With either style of chamber, trained technicians control pressurization and times of delivery of the oxygen from a control panel outside the chamber (Figure 4). Communication is maintained with a technician or nurse who stays with the patients in the chamber by means of an intercom system, and the hyperbaric physician remains readily available at all times during treatments.

MECHANISMS OF ACTION: THE PHYSICS OF HBOT It is the delivery of inhaled compressed oxygen to a system under pressure that elevates tissue oxygen tension to therapeutic levels. Topical delivery of oxygen

FIGURE 1. Monoplace chamber, an acrylic single-person chamber filled with 100% pressurized oxygen.

FIGURE 2. Multiplace chamber, a tree-standing metal cylinder that has been described as resembling a submarine.

in limb chambers does not provide the therapeutic rise in tissue oxygen tension because the alveolar membrane needed for diffusion of oxygen into the blood is present only in the lungs. The three laws of physics that explain how HBOT works are those of Boyle, Henry, and Dalton. Boyle's Law states that when the temperature is constant, the volume of a gas is inversely proportional to its pressure; this explains the effectiveness of HBOT in treating the gas bubbles

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FIGURE 3. In a multiplace chamber, the patient breathes oxygen through a hood or mask.

sults in a doubling of the amount of dissolved gas. The partial pressure law, or Dalton's Law, states that the total pressure of a mixture of gases is the sum of the individual partial pressures of each gas. For example, air is commonly considered to be a mixture of 21% oxygen and 79% nitrogen. The total pressure of these two gases is 760 m m H g at sea level (1 atmosphere absolute, or 1 atm). The partial pressure of oxygen in air is thus 760 x 21 + 100, or 160 m m Hg. Each 33 feet of seawater equals 1 atm, or the pressure exerted b y the atmosphere at sea level. The partial pressure of 100% oxygen at 3 atm (the equivalent pressure exerted by the atmosphere plus 66 feet of seawater) equals 2280 m m Hg of oxygen (3 x 760 x 100 - 100 = 2280). This illustrates the tremendous increase in oxygen available to the b o d y while breathing 100% oxygen under 3 atm of pressure.

CLINICAL EFFECTS AND IMPLICATIONS

FIGURE 4. Trained technicians control pressurization and times of delivery of the oxygen from a control panel outside the chamber.

formed with the bends and other gasproducing disease entities. Higher ambient pressures cause smaller bubbles, relieving the physical pressure on nerves and blood vessels caused by the bubbles and lessening subsequent damage to b o d y tissues. The increases in plasma concentrations of oxygen that are seen with HBOT can be explained by Henry's Law. This law states that the amount of gas dissolved in a solution is directly proportional to the pressure; a doubling of the pressure re-

The therapeutic effects of HBOT derive from either primary or secondary effects of hyperoxygenation. The primary effect of HBOT is a tremendous increase in the amount of oxygen dissolved in the plasma, providing increased oxygen to all tissues with positive plasma flow. In human beings, approximately 97.5% of the oxygen in the blood is carried by hemoglobin, with the remaining 2.5% dissolved in the plasma. 3 With the b o d y in the resting state, as blood passes from the arterial to the venous side of the capillary bed approximately 5% of oxygen by volume is extracted from hemoglobin. This amount is sufficient to support normal cellular function. At pressures of 3 atm or 66 feet of seawater, breathing 100% oxygen will raise the plasma concentrations of dissolved oxygen to 6.9% b y volume. This more than meets the tissue needs of the 5% b y volume normally extracted from hemoglobin and explains w h y HBOT can sustain tissue function in the absence of hemoglobin. A clear understanding of these effects can assist ET nurses to determine which patients m a y benefit from HBOT. Patients with acute blood loss anemia have a marked reduction in the number of circulating erythrocytes and therefore in the amount of hemoglobin available for

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the transport of oxygen. Increasing the oxygen dissolved in the plasma can sustain tissue function until the hemoglobin can be replaced, either by transfusion or by the body's own restorative processes. HBOT is an effective antidote for carbon monoxide poisoning. Accidental or intentional exposure to carbon monoxide is a hazard in all parts of the country. Carbon monoxide has a binding affinity with hemoglobin 200 times greater than the binding affinity of the oxygen molecule. Carbon monoxide-bound hemoglobin (carboxyhemoglobin) is unavailable to the body for the transport of oxygen. The half-life of carboxyhemoglobin is 5.5 hours in the person breathing room air at sea level (1 atm). Breathing 100% oxygen at 3 atm (chamber depth of 66 feet of seawater) can decrease this half-life to just 23 minutes. In addition to this effect, the high levels of plasma-dissolved oxygen found with HBOT can help maintain tissue viability and prevent neurologic deficits in patients with carbon monoxide poisoning. The increased amount of dissolved oxygen in the plasma produced by HBOT can aid in clinical situations that feature a positive plasma flow but reduced transport of the cellular components of blood (e.g., erythrocytes and hemoglobin). One example is radiation damage, which causes swelling, cellular breakdown, and necrosis of the endothelium, resulting in a narrowing of the blood vessel lumen and obstruction to transport of the cellular components of the blood. The high concentration of oxygen carried in the plasma during HBOT is available to tissues for metabolism and aid in tissue preservation. Treatment of patients with radiation damage has proved beneficial in helping tissues to heal because of the positive plasma flow. Any patient needing an operation in a previously irradiated area of the body should undergo a course of HBOT before and after surgery to promote healing. The secondary effects of HBOT are related to edema reduction and vasoconstriction (offset by high plasma oxygen levels). High oxygen tension has bacteriocidal and bacteriostatic effects, reduces the size of bubbles in the tissue (as with air embolism and decompression sickness), and stimulates angiogenesis in wounded tissue. HBOT can maintain tissue oxygenation

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in conditions such as interstitial edema that increase the distance between the capillary and target tissue. Obstruction of the microcirculation for any reason (e.g., crush injury) causes a reduced circulation of the cellular components of blood, even though plasma circulation may still occur. Hyperoxygenation is beneficial because it increases the diffusion of oxygen from the plasma. There is a well-established distance across which oxygen can be expected to diffuse from the capillary to the tissue. If the distance between the capillary and the tissue is greater than the diffusion distance of the oxygen, the tissues will become hypoxic. Oxygen diffusion through tissue fluids is proportional to the square root of the amount of oxygen in the capillary. If the amount of oxygen is increased tenfold, the diffusion distance increases by a factor of the square root of 10, or approximately three times. 4 Increasing the plasma concentrations of oxygen by HBOT therefore helps to preserve tissue oxygenation and reduce hypoxia. Hyperoxygenation can cause vasoconstriction, which helps to reduce edema and tissue congestion. The combined effects of increased tissue oxygenation and reduced edema as a result of vasoconstriction helps to explain the beneficial effects of HBOT in management of compromised grafts and flaps. Despite the increased plasma concentration of oxygen, a severely ischemic wound, as evidenced by a low ankle-tobrachial index, has little chance of healing unless bypass grafting or angioplasty is accomplished before initiation of HBOT. 5 Such correction of an underlying problem can prevent further tissue damage and enhance the patient's ability to remained healed. A significant benefit of hyperoxygenation is its impact on bacteria. HBOT has been found to have bacteriostatic and bactericidal effects on anaerobic bacteria. In particular, HBOT has been found to have a bactericidal effect on gas-forming clostridial organisms such as those causing gas gangrene. The high tissue oxygen tensions produced by HBOT can inhibit the toxins produced by the synergistic bacteria found in necrotizing fasciitis (Staphylococcus aureus and Bacteroides). These effects support the role of HBOT as a lifesaving and limb-preserving adjunct therapy for these conditions. HBOT can also contribute to control of

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Despite the increased plasma concentration of oxygen, a severely ischemic wound has little chance of healing unless bypass grafting or angioplasty is accomplished before initiation of HBOT.

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It is clear that HBOT can play a role in the management of wounds with a c u t e or chronic infection.

aerobic infections. Theoretically, the hyperoxic state induced by use of HBOT should support the growth of aerobic bacteria. In the clinical setting, however, this is only partially true because the expected proliferation of aerobes is counteracted by the stimulation of leukocyte activity caused by high oxygen levels. HBOT contributes to infection control because the oxidative burst mechanism necessary to kill bacteria is oxygen dependent; although neutrophils may be able to engulf bacteria under hypoxic conditions, they cannot kill bacteria without oxygen. Infection control by means of organismspecific antibiotics is an important factor to consider in any wound management plan. The antimicrobial effect of some antibiotics, in particular the aminoglycosides, can be enhanced by the use of HBOT. Hypoxic states inhibit the transport of the aminoglycosides into the bacteria. HBOT reduces the hypoxia, which enables the aminoglycosides to reach the target bacteria. 6 It is clear that HBOT can play a role in the management of wounds with acute or chronic infection, such as necrotizing fasciitis, gas gangrene, or chronic refractory osteomyelitis. For many situations, HBOT is used in conjunction with surgical debridement of necrotic tissue and organism-specific antibiotic therapy to accomplish the goals of infection control and wound repair. Hyperoxygenation also affects glucose and insulin metabolism in persons with diabetes. It has been documented that blood glucose levels decrease in persons with insulin-dependent diabetes undergoing HBOT, and insulin requirements may change rapidly. If possible, these patients should be placed on sliding-scale doses, with frequent checks of capillary blood glucose levels. 7 Control of blood glucose levels is an important aspect of support for wound healing in persons with diabetes. High glucose levels can cause leukocyte dysfunction and may contribute to the infections seen in these patients. Persons with diabetes have an impaired wound healing mechanism. These patients have impaired collagen synthesis and wound contraction with delayed epidermal migration. The thickening of the capillary basement membrane (so called "small-vessel disease") is not the primary reason for the ischemia seen in this population; rather, it is obstruction

in the larger vessels that causes ischemia. Patients with diabetes and ischemic lesions should be referred for vascular evaluation and correction of any underlying vascular occlusion, s In patients with nonhealing, chronic, or "problem" wounds, HBOT has been shown to promote healing by intermittently increasing oxygen tension. HBOT stimulates fibroblast proliferation and collagen synthesis, which provides a support network for the growth of new capillaries (angiogenesis). 9 Macrophages are the first cells to enter the dead space of a wound, but they are inactivated by oxygen levels less than 30 mm Hg. 1° They are responsible for secreting factors involved in the proliferation of fibroblasts, smooth muscle cells, and endothelial cells. The angiogenesis factor secreted by the macrophage is responsible for stimulating the budding of endothelial cells and capillary ingrowth. Fibroblaststimulating factor secreted by the macrophages causes fibroblasts to move in to the wound within 24 hours of initial injury. Fibroblasts are responsible for the production of proteoglycans and tropocollagen (a collagen precursor). Tropocollagen requires ferrous iron, a reducing agent (e.g., ascorbic acid), ~-ketoglutarate, and oxygen to be transformed into insoluble collagen. 1° In experimental wound models most of the proliferative fibroblasts are found in areas where oxygen tensions have been measured at about 40 m m Hg. 11HBOT has been found to promote angiogenesis by providing oxygen to macrophages and fibroblasts. 9-~4 Patients are warned that their wounds will turn bright red, but they are reassured that this is a positive sign indicating wound healing. Many patients mistakenly think that a heavy yellow fibrin coat or dark eschar covering the wound means that the wound is scabbing over and healing. HBOT alone is not the "magic bullet" of wound healing. In addition to appropriate topical therapy, control of infection, and control of blood sugar levels in persons with diabetes, wound healing also requires adequate nutrition. One aspect of proper nutritional status is a positive nitrogen balance, as evidenced by serum albumin levels of 3.3 to 4.5 gm/dl. ~5 Although positive nitrogen balance is not in itself a prognosticator of wound healing, it is an indicator of adequate nutrition. TM

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Protein is a component of antibodies and lymphocytes that is necessary for their proper function. Calories are needed to provide the energy necessary for tissue defense and w o u n d repair. Vitamin C is essential for collagen synthesis and maintenance of capillary wall integrity. Vitamin A can help patients who are taking steroids by partially counteracting the adverse effects of steroids on w o u n d healing by restoring the local inflammatory response and epithelial migration stimulus. Vitamin B complexes and copper are needed for collagen fibers to cross-link. Iron is a necessary component of hemoglobin and is also needed for collagen synthesis. Zinc is needed for collagen formation and protein synthesis. 15

INDICATIONS The a p p r o v e d indications for HBOT, as proposed by the Undersea and Hyperbaric Medical Society (UHMS), are listed in Box 1. Indications of particular relevance to ET nursing practice are italicized. A n y ET nurse caring for patients with one of the italicized indications should consider referral for HBOT evaluation. Selection of patients for HBOT is based on numerous factors. These factors include UHMS-approved indications for HBOT (Box 1), the potential for rehabilitation and return to function, and physical considerations, which m a y include vascular studies, bone scans, radiographs, and transcutaneous tissue oxygenation measurements. If the underlying factor causing or contributing to a w o u n d is not corrected, the potential for recurrence remains and HBOT m a y not be indicated for that patient. When considering HBOT for a nonhealing wound, it is essential to determine whether ischemia is a contributing factor in the failure to heal and whether there is plasma flow to the wound. If the failure to heal is caused by unrelieved pressure or uncorrected malnutrition, HBOT is contraindicated. HBOT is also contraindicated in w o u n d s that lack plasma flow (e.g., severely ischemic necrotic wounds), because HBOT exerts its therapeutic effects by hyperoxygenation of the plasma. To affect tissue oxygen tension, there must be delivery of the hyperoxygenated plasma to the target tissue. Management of patients with isch-

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emic lesions must include vascular assessment and possibly revascularization, because increasing the blood supply to the w o u n d bed raises the likelihood that HBOT will promote w o u n d healing. Ethical considerations, such as do-notresuscitate status, must be considered in light of the potential benefit of HBOT. If HBOT can positively affect or correct the process causing the do not resuscitate order, a joint decision of patient (if possible), family, and medical personnel can be made. The patient also must be evaluated for potential benefit versus the higher metabolic d e m a n d s placed on the b o d y by stimulation of w o u n d healing with HBOT. A healthy 20-year-old will tolerate the metabolic stresses much better than will a chronically debilitated patient. Physical d e m a n d s are evaluated because the patient must be able to tolerate moving from bed to a stretcher or wheelchair at least twice per treatment, from the room to the chamber and back.

CONTRAINDICATIONS There are m a n y contraindications to HBOT. Two contraindications not specifically dealt with in this article include hereditary spherocytosis and optic neuritis. One gender-specific contraindication is pregnancy; w o m e n who are or who m a y be pregnant should have a pregnancy test before initiation of HBOT. If the test result is positive, HBOT is not recommended because the effects of high concentrations of oxygen are undetermined in the h u m a n fetus, and ethical considerations prevent clinical research in this area. Certain medications have been found to have adverse reactions when combined with HBOT, and use of these drugs is a relative contraindication. Patients receiving these medications are considered candidates for HBOT only if the medication can be safely discontinued for the duration of the course of HBOT. Upton and coworkers 17 investigated the use of HBOT as a possible nonsurgical treatment for extravasation damage of doxorubicin (Adriamycin). They found an 87% mortality rate among rats exposed to HBOT, probably related to cardiac toxicity. HBOT for patients receiving doxorubicin should be delayed for 1 week after the last dose to avoid this toxic effectJ 8

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When considering HBOT for a nonhealing wound, it is essential to determine whether ischemia is a contributing factor in the failure to heal and whether there is plasma flow to the wound. B

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Transcutaneous oxygen pressure can also be used to evaluate wound healing potential.

The production of superoxide dismutase (the body's major protection against oxygen toxicity and seizures) is blocked by disulfiram (Antabuse). A single HBOT exposure (e.g., for carbon monoxide poisoning) While taking this drug would be safe, but continued exposure to HBOT would be risky because of blocking the superoxide dismutase. The anticancer agent cis-platinum affects DNA synthesis and thereby delays production of fibroblasts. HBOT may increase cis-platinum's cytotoxic effects and therefore may worsen wounds in patients taking this drug. Mafenide acetate (Sulfamylon) is a carbonic anhydrase inhibitor that can cause carbon dioxide buildup in the tissues, which results in peripheral vasodilation. In conjunction with the central vasoconstriction caused by HBOT, severe adverse side effects may occur. Patients referred for HBOT who use mafenide acetate are switched to silver sulfadiazine because this drug is comparable to mafenide acetate but does not carry the same risks to the tissues. Patients with diseases of the pulmonary system causing blebs should be evaluated very carefully before HBOT therapy. Blebs may rupture while under pressure and develop into a pneumothorax. Left untreated, a pneumothorax can continue to enlarge at depth and may become a tension pneumothorax. If this occurs, decompression is dangerous and may be life-threatening because of the continued expansion of the gases during decompression (Boyle's law). For patients with a known pneumothorax, placement of a chest tube is necessary before HBOT. It is extremely important that radiographs be evaluated for pneumothorax after placement or attempted placement of a central line.

INITIAL ASSESSMENT In addition to the chest radiograph and general medical evaluation, patients who are undergoing HBOT are screened for potential seizure activity, history of pneumothorax, and unexplained high fevers. Often, vascular workups are done to establish the potential for limb salvage. The most frequent procedures done to evaluate limb viability are noninvasive vascular studies and transcutaneous oxygen pressure studies.

Transcutaneous oxygen pressure studies provide an unbiased evaluation of local tissue perfusion and oxygenation. Measurements are made by attaching an electrode to the skin near the wound site. The electrode is heated to 44 ° C to provide for capillary dilation and maximize the oxygen diffusion through the skin. A control site, usually on the patient's chest, is selected and another electrode is attached. Measurements are usually made at 10, 20, and 30 minutes. Two sets of measurements are made before exposure to HBOT, the first with the patient breathing room air and the second made with the patient breathing 100% oxygen. A third set of measurements is obtained after the patient has been pressurized to the treatment depth and has started to breathe 100% oxygen. Transcutaneous oxygen pressure can be used to evaluate w o u n d healing potential. Most transcutaneous studies are done on questionably ischemic lower limbs to predict tissue viability and to help determine amputation levels. Tissue measurements below 30 m m Hg are indicative of poor oxygenation in the affected area. These patients are at higher risk for healing problems and may benefit from the extra oxygenation provided by HBOT. Burgess and associates 19 found that in using transcutaneous oxygen pressure values to select amputation levels, they had 100% healing of the below-knee amputation stump in patients with transcutaneous oxygen pressure levels of 40 m m Hg. Only 15 patients in a series of 19 patients with transcutaneous oxygen pressure values of more than zero but less than 40 m m Hg had healing at the original amputation site.

TREATMENT PROTOCOLS Patients are typically treated once per day and may be exposed to HBOT twice or more per day, depending on the severity of the underlying disease process. Treatment time consists of time to pressurize and depressurize the chamber and 90 minutes of oxygen breathing, broken up into two 45-minute or four 20-minute sessions with 5-minute air breaks interspersed. Total treatment time is approximately I hour 45 minutes per session, but the sessions are individually tailored to patient need. Some patients at high risk may initially receive as many as four to

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six treatments per day during an acute crisis, whereas other patients may undergo one HBOT session per day. These determinations are based on the nature of the problem, physician recommendation, and patient tolerance. The cost for treatment is approximately $450 per session. Physician charges are billed separately and vary by doctor. Most insurance companies, Medicare, and Medicaid will reimburse for these treatments if used for approved indications as outlined in Box 1. There are numerous less expensive methods of treating wounds, but for some patients HBOT is a useful adjunct in w o u n d healing. 2°

HBOT AND WOUND DRESSINGS Topical therapy for w o u n d care has been covered in numerous other articles and texts. 2° In relation to HBOT, however, some consideration must be given to the makeup of the dressing. Hyperbaric environments are by nature subject to high levels of oxygen, and prevention of fire hazards and control of flammable material are of prime concern to the HBOT staff. ET nurses should help preserve a safe environment for patients undergoing HBOT by careful selection of topical dressing materials. HBOT patients are routinely screened before each treatment for cigarette lighters and matches (ideally, these patients should stop smoking) and are told to refrain from wearing alcohol- and petroleum-based cosmetics, lotions, and hair care products for the duration of their treatment. This can present a challenge to the ET nurse because dressing materials also may contain some of these products. This is particularly critical in the monoplace environment, which is pressurized with 100% oxygen. In recommending dressings, it is necessary to remember to eliminate or strictly limit ointments and skin care products containing petroleum or alcohol. Often these products are applied sparingly after the last HBOT treatment of the day and removed before the initial HBOT treatment on the following day. Hydrocolloids, calcium alginates, hydrogels, thin film, thin foam dressings, and normal saline solution-soaked gauzes are usually safe for the HBOT environment.

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Box 1

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Approved indications for HBOT

• Air or gas embolism • Carbon monoxide complicated by cyanide poisoning • Clostridial myonecrosis (gas gangrene) • Crush injury, compartment syndrome, and other acute traumatic ischemias • Decompression sickness (the bends) • Enhancement of healing in selected problem wounds • Exceptional blood loss ( a n e m i a ) • Necrotizing soft-tissue infections (subcutaneous tissue, muscle and fascia) • Osteomyelitis (refractory)

• Radiation tissue damage (osteoradionecrosis) • Skin grafts a n d flaps (compromised) • Thermal burns Indications in italics are of particular interestto ETnurses.

Box 2. U H M S headquarters The Undersea and Hyperbaric Medical Society 10531 Metropolitan Ave. Kensington, MD 20895 Phone: 301-942-2980

POTENTIAL RISKS AND SIDE EFFECTS Barotrauma is probably the most frequent side effect of HBOT. It can occur in any gas-containing cavity of the body with rigid walls, such as the inner ear and sinuses. The patient must be able to equalize the inner ear pressure during pressurization by performing the Valsalva maneuver. Failure to equalize initially creates a feeling of pressure or discomfort, known as a "squeeze." Continued failure to equalize can cause actual barotraurna. The medical, nursing, and technical support staff working with the patients are trained to recognize and intervene as necessary to prevent barotrauma. Sinus barotrauma is treated with antihistamines and decongestants. Most patients undergoing HBOT will be able to successfully perform the Valsalva maneuver to equalize inner ear pressure during pressurization of the chamber. Patients who are unable to perform this maneuver, have tracheostomy or nasogastric tubes, are intubated, or have altered levels of consciousness may require placement of pressure equalization tubes by an otolaryngologist. All pa-

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HBOT is not a "magic bullet" for nonhealing wounds, nor is it without risk.

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tients must have a recent chest radiograph that demonstrates no pneumothorax. If left untreated, a pneumothorax could cause serious complications during decompression of the HBOT chamber. Patients are screened for history of seizure activity because elevated oxygen toxicity may precipitate a seizure. Febrile states can also make a patient more susceptible to seizure activity. Prolonged use of adrenal corticosteroids has been found to potentiate oxygen toxicity. An increase in epinephrine and adrenocortical hormones in response to the stresses of the hyperbaric environment seems to sensitize the patient to oxygen toxicity and seizures. Pulmonary oxygen toxicity may be a consideration in patients maintained on an inspired oxygen fraction of greater than 40% between HBOT sessions. In this situation, respiratory therapy and the pulmonologist need to be aware of the HBOT to monitor for toxicity and intervene as needed. Confinement anxiety or claustrophobia can also be a problem for patients undergoing HBOT. It is not as great a consideration in the multiplace chamber as in the monoplace chamber. Patients in monoplace facilities that have had claustrophobic problems in a magnetic resonance imaging chamber may be reluctant to be placed in the HBOT chamber. In the multiplace chambers, patients may have tolerance problems with the hood or face mask used for oxygen delivery. If HBOT is considered to be an integral part of the necessary therapy for a particular patient, a mild sedative may be considered to help alleviate anxiety. Occasionally patients notice visual changes of uncertain origin during a course of HBOT. Most patients notice an ability to read without their reading glasses (resolution of presbyopia), but they experience an increased difficulty in focusing on distant objects (myopia). Patients are informed that this is only temporary and that their vision will probably return to pre-HBOT levels within about 6 weeks after stopping treatments. In some persons, however, a return to pretreatment visual acuity may not occur. The HBOT staff should discuss potential risks and side effects with patients before starting treatments.

CONCLUSION H B O T is n o t a " m a g i c b u l l e t " for non-

healing wounds, nor is it without risk. When used for appropriate patients in conjunction with a total wound management approach, however, it can contribute significantly to tissue and limb salvage. It is important for ET nurses to be knowledgeable regarding this treatment modality so that they can refer patients appropriately and modify topical therapy when indicated. Dr. Leon Greenbaum, president of the UHMS, has given permission for ET nurses to contact the UHMS headquarters for assistance with questions regarding the possibility of referral for HBOT and the location of the nearest center providing HBOT (Box 2). After location of the nearest facility, specific questions can be directed to that facility for appropriateness of referral and methods to obtain their services for patients. I acknowledge Our Lady of the Lake Regional Medical Center, the staff of the OLOL Hyperbarics department, Dr. Leon Greenbaum and the UHMS. I also wish to acknowledge the Emory University Wound, Ostomy and Continence Nurses Education Program and especially Dorothy Doughty for her encouragement and assistance in preparation of this article.

REFERENCES 1. Jain KK. Textbook of hyperbaric medicine. Lewiston, New York: Hogrefe and Huber, 1990:5-7. 2. Boerema I, Meyne NG, Brummelkamp WK. Life without blood: a study of the influence of high atmospheric pressure and hypothermia on dilution of blood. J Card iovasc Surg 1960;1:133-46. 3. Strauss MB. Wound hypoxia. Curr Concepts W o u n d Care 1986;9(4):16-9. 4. Strauss MB, Improving host responsiveness by hyperoxygenation. Curr Concepts W o u n d Care 1987;10(3):15. 5. Kindwall EP, Gofflieb LJ, Larson DL. Hyperbaric oxygen therapy in plastic surgery: a review article.Plast Reconstr Surg 1991;88:898-908. 6. Park MK, Muhvich KH, Myers RAM, Marzella L. Effects of hyperbaric oxygen in infectious diseases: basic mechanisms. In: Kindwall EP, ed. Hyperbaric medicine practice. Flagstaff,Arizona: Best Publishing, 1994:142, 156. 7. Kindwall EP. The use of drugs under pressure. In: Kindwall EP, ed. Hyperbaric medicine practice. Flagstaff,Arizona: Best Publishing, 1994:256. 8. Matos LA, Nunez AA. Enhancement of healing in selected problem wounds. In: Kindwall EP, ed. Hyperbaric medicine practice. Flagstaff, Arizona: Best Publishing, 1994:595.

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9. Hunt TK, Zederfeldt B, Goldstick TK. Oxygen and healing. A m J Surg 1969;I 18:521-5. 10. Cooper D. The physiology of w o u n d healing: an overview. In: Krasner D, ed. Chronic w o u n d care. King of Prussia, Pennsylvania: Health Mana g e m e n t Publications, 1990:6-8. 11. Stephens OF, Hunt TK. Effect of changes in inspired oxygen and carbon dioxide tensions on w o u n d tensile strength: an experimental study. A n n Surg 1971;173:515-9. 12. Hunt TK. The physiology of w o u n d healing. Ann Emerg M e d 1988;17:1265-73. 13. Hunt TK, Pal MP. The effect of varying ambient oxygen tensions on w o u n d metabolism and collagen synthesis. Surg Gynecol Obstet 1972;135: 561-7. 14. Roberts GP, Harding KG. Stimulation of glycosaminoglycan synthesis in cultured fibroblasts by hyperbaric oxygen. Br J Dermatol 1994;131: 630-3. 15. Konstantinides NK. Principles of nutritional support. In: Bryant RA, ed. Acute and chronic wounds nursing management. St Louis: MosbyYear Book, 1992:44-5. 16. HillDP, Cooper DM, Robson MC. Serum albu-

min is a poor prognostic factor for pressure ulcer healing in controlled clinical trials. Wounds 1994;6:174-8. 17. Upton PG, Yamaguchi KT, Meyers S, Kidwell TP, Anderson RJ. Effects of antioxidants and hyperbaric oxygen in ameliorating experimental doxorubicin skin toxicity in the rat. Cancer Treat Rep 1986;70:503-7. 18. Kindwall EP. Contraindications and side effects to hyperbaric oxygen treatment, In: Kindwall EP, ed. Hyperbaric medicine practice. Flagstaff, Arizona: Best Publishing, 1994:46. 19. Burgess EM, Matsen FA, Wyss CR, Simmons CW. Segmental Transcutaneous measurements of PO 2 in patients requiting below-the-knee amputation for peripheral vascular insufficiency. J Bone Joint Surg [Am] 1982;64A:378-82. 20. Grim PS, Gofflieb LJ, Boddie A, Batson E. Hyperbaric oxygen therapy. J A M A 1990;263:221620. 21. Wiseman DM, Royce DT, Alvarez OM. W o u n d dressings: design and use. In: Kelman C, Diegelm a n n RF, Lindblad W J, eds. W o u n d healing: biochemical and clinical aspects. Philadelphia: W B Saunders, 1992:562-80.

EDITOR'S C O M M E N T HBOT: Anecdote or Science?

ceived by some to be a qualitative phenomenon or the research that challenges the effectiveness of specific therapies and suggests others is not read, is rejected, or remains unknown to the clinician. In 1983, Rudolph, referring to the plethora of approaches to w o u n d care, wrote, "Many of these agents even though there is no sound physiologic basis for their having any efficacy, do in fact provide improved w o u n d care. "1 The principle underlying this notion is manifested best by a research methodologic consideration known as the "Hawthorne effect." This concept evolved after a series of studies undertaken some years ago at the Hawthorne plant of the Western Electric Corporation. Employees there were subjected to multiple changes in working conditions; lighting was dimmed or made brighter, working hours were arranged in novel patterns, and other changes were made. Regardless of what change was introduced, the productivity of the workers in the plant increased. The overall conclusion from the study, and one that resulted in establishing a gold standard for research design, was that investigations needed to employ randomization. The findings from Hawthorne demon-

Regarding anecdotal reports, Peter Medawar once stated, "Induction is the arguing from the particular to the general and it expands our pretension of knowledge." With respect to the four ways of knowing--tenacity, authority, a priori, and the method of science--it is clear which level of knowledge should be the goal of the scientist. Science has been defined as a w a y of knowing that holds up to public scrutiny; that is, the same conclusions could be drawn from the results of an investigator's study by "any person" capable of understanding them. Despite our desire for this level of objectivity in knowledge, those of us involved in the care of patients with wounds continue to be aware of the frequent use of case reports, case series, and anecdotal "testimonials" as means of supporting approaches to the care of patients with both acute and chronic wounds. Some of this can be explained by the difficulties inherent in objectively measuring the effects of treatments in human beings given our current technologic and scientific capabilities. Other treatments, sad to say, continue because the w o u n d is not per-

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