Physiologic effects

UV light does not heat tissue. Instead, it is believed to alter cellular function, increase cell wall permeability through altering the shape of proteins, stimulate production of various chemicals such as prostaglandins and arachidonic acid, and increase the production of adenosine triphosphate (Camp et al, 1978). The erythema that results increases local vasodilation, tissue oxygenation, and histamine release. Earlier studies using high doses of UV report increases in epithelialization and epithelial cell turnover (Freytes et al, 1965; Wills et al, 1983), increased granulation tissue growth and tissue perfusion at lower doses (Ramsay and Challoner, 1976), stimulated growth factor release (James et al, 1991), and increased autolysis (Kloth, 1995). However, these older studies used a different standard of care for comparison than exists today. Therefore, whether UV enhances wound healing in conjunction with advanced wound healing approaches is not known.

Each form of UV has different effects on tissue. UV-A and UV-B are nonionizing. They are both found environmentally, as they pass through the atmosphere. UV-A produces a mild erythema, whereas UV-B elicits a stronger erythematous response while it penetrates the epidermis. The impact of UV-A can be increased with the use of oral psoralens, a photosensitizing agent, before treatment. UV-A penetrates several millimeters into the skin, the deepest of the three forms. UV-B produces hyperplasia of the dermis and stratum corneum 3 days after treatment and has been used to toughen scars (Parrish et al, 1981).

UV-C is mutagenic but is not linked to skin cancers for several reasons: (1) UV-C only penetrates the most superficial layers of the epidermis; (2) the superficial layers of epidermis are sloughed often enough to prevent development of neoplasms; and (3) naturally occurring UV-C is blocked by the atmosphere before it reaches the earth’s surface. However, as wound treatment exposes the more permanent healing tissue, and not the epidermis, to UV-C radiation, the long-term cancer risk is unknown. UV-C is recognized to be germicidal, which has come to be the primary use for UV treatment. Other evidence suggests that UV-C can increase epithelialization, increase epithelial cell turnover (Freytes et al, 1965), increase granulation tissue growth and tissue perfusion at lower doses (Ramsay and Challoner, 1976), stimulate growth factor release (James et al, 1991), and increase autolysis (Kloth, 1995; Spielholz and Kloth, 2000).

The bacteriocidal effects of UV have been recognized for more than a century (Gates, 1928). UV-C has been demonstrated to kill methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin-resistant enterococcus (VRE) in vitro in 90 seconds (Conner-Kerr et al, 1999). The mechanism of action is theorized to be inhibition of DNA synthesis (Hall and Mount, 1981). Another in vitro study (Sheldon et al, 2005) found MRSA eradication with use of UV-C, with an even greater impact on Pseudomonas. A case series by Thai et al (2002) demonstrated reduced bacterial counts and more rapid healing with UV-C use, although treatment was not standardized and there was no control, which limit the ability to connect use of UV to the improvements observed. Thai et al (2005) later studied the effect of one 180-second UV-C treatment session on semiquantitative swab culture results of 22 patients whose chronic ulcers contained high levels of bacteria and exhibited signs of infection. Types of wounds included pressure, venous, diabetic, and arterial etiologies. Results showed a statistically significant reduction of the predominant bacteria and significant reductions of MRSA and S. aureus.

Indications and use

Because of its antimicrobial effects, UV-C is sometimes used in operating rooms in place of laminar flow to reduce surgical infections (Ritter et al, 2007). Following a systemic review, Reddy et al (2008) did not recommend UV treatment of pressure ulcers. However, international guidelines for treatment of pressure ulcers (EPUAP-NPUAP, 2009) advocate the consideration of UV-C treatment in the short term for pressure ulcers that do not respond to traditional therapies or as adjunctive therapy to reduce bioburden in clean, critically colonized Stage III and IV pressure ulcers. Pressure ulcer guideline recommendations related to UV are based on expert opinion and small in vitro and in vivo studies (Conner-Kerr et al, 1998, 1999; Thai et al, 2005). The guideline further states that UV should not be used in the absence of additional appropriate therapies due to insufficient evidence to draw definitive conclusions (EPUAP-NPUAP, 2009).

A common protocol involves the application of petrolatum to the periwound and a towel or sheet drape to the surrounding areas to prevent UV absorption. Limited evidence supports periwound UV treatment for promoting wound closure. The lamp is kept 1 inch from the wound, perpendicular to the skin surface. Treatment is provided for 90 to 120 seconds. Treatment should be discontinued when the bioburden is adequately reduced. Both the patient and the clinician must wear UV-blocking eye protection. Even if a person does not look directly at the light, the waves may bounce off surfaces and reflect into the eye, causing damage.

Contraindications and precautions

Safe and effective dosage of UV-C may vary based on the distance from the light source, the intensity of the light source, and the size of the treated area. UV-C has a very low risk of causing burns. Contraindications, precautions, and conditions that can be exacerbated by UV treatment (especially with UV-A or UV-B over large areas of the body) vary according to the source (Box 24-1). Conditions and medications requiring the clinician to use caution when applying UV treatment are listed in Box 24-2 (Cameron, 2008; Michlovitz and Nolan, 2005).

Traditional high-frequency ultrasound (1.0–3.3 mhz)

Traditional clinical therapeutic applications use a frequency of 1 or 3.3 MHz. The user may elect to use a duty cycle. This parameter results in pulsing of the current, with periods of wave production followed by quiet periods. A 20% duty cycle is most commonly used, in which the sound waves are on for 1 ms and then off for 4 ms. Heat is produced but is dispersed so quickly that no temperature change occurs in the tissue. Ultrasound has been used to promote soft tissue healing for more than 6 decades, primarily for orthopedic conditions. More recently, that use has extended to wound healing.

An ultrasound device consists of the control unit and the hand-held sound head, or transducer (Figure 24-2). The user is able to control the intensity (amount of power used), whether the waves are continuous or pulsed, the duration of treatment, and, on some units, the wavelength. The device runs electricity through a crystal in the sound head, causing the crystal to vibrate through a reverse piezoelectric effect. These vibrations create sound waves that pass through the sound head membrane and into the tissue. These waves elicit both thermal and nonthermal effects.

FIGURE 24-2 A, Ultrasound device. B, Close-up of ultrasound parameter settings.

(Courtesy Renee Cordrey.)