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DEPARTMENTS: Editorial

Patient Turning Schedules: Why and How Often?

Salcido, Richard “Sal MD

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Advances in Skin & Wound Care: May 2004 - Volume 17 - Issue 4 - p 156

For years, we have been advised to turn our patients at least every 2 hours to prevent tissue breakdown. This axiom has been passed down uncritically through generations of wound care practitioners.

It is time to look more closely at this practice. Is turning patients every 2 hours really enough? Or should we be turning them more often? Where did the 2-hour timeframe originate? How often is it being followed in practice?

Although answering all of these questions is beyond the scope of this editorial, I want to address the origin of the 2-hour turning rule.

Pathomechanical Forces at Work

Unrelieved pressure is a well-known clinical risk factor for pressure ulcer development. However, pressure is not the only mechanical influence that contributes to tissue failure and, ultimately, breakdown. Other factors that contribute to pressure ulcer development fall under the rubric of pathomechanics, including pressure, friction, shear, and moisture.

Pathomechanics implies noxious mechanical application to the body, such as shear and axial pressure. Theoretically, prolonged pressure leads to ulceration if it exceeds tissue capillary pressure, generally accepted as 32 mm Hg in the arteriolar limb. 1–4 Although critically influenced by body contour, tissue stiffness, and composition, pressures under 32 mm Hg are assumed by many clinicians to be safe. This benchmark is further defined as interface pressure. Products aimed at reducing or relieving pressure have tended to use interface pressure as the standard for judging product efficacy. 5

Tissue Under Pressure

The critical interface pressure is the pressure above which tissue cannot be loaded for an indefinite period without resulting in ulceration. Pressure and the duration of pressure application necessary to cause an ulcer have an inverse relationship: Unrelieved axial pressure 4 to 6 times systolic causes necrosis in less than 1 hour; pressure below systolic might not cause similar lesions for as long as 12 hours.

Kosiak 1, Husain 6, and Dinsdale 7 quantitatively verified this hyperbolic relationship in dogs, rats, and pigs. The concept of a critical interface pressure, then, is specific to animal models. This early animal research led to the practice of turning patients every 2 hours, and was advanced in humans with the work of Reswick and Rogers 8 in 1976.

How do other components of the pathomechanical cascade, such as shear, factor into the every-2-hour rule? Shear exacerbates the tendency to ulcerate as a result of axial forces. Dinsdale 7 determined, again in animal models, that continuous shear directed to a site of constant axial pressure lowered the ulceration threshold sixfold. Shear forces, for example, can be important for sacral pressure ulcer formation. It is logical to conclude that while patients are in the semi-upright position in bed, the downward angular and vertical forces tend to distort tissues and blood vessels near the sacrum, placing this region at risk for tissue breakdown. 9

A Challenge

The majority of what we know about pathomechanics associated with pressure ulcer development is based on incomplete information, with a strong influence from animal wound models. As technology advances and newer devices for analyzing tissue relief and turning frequency evolve, we must exploit the opportunity to enhance our knowledge.

The 2-hour turning rule needs to be challenged with research. Turning frequency lacks the strength-of-evidence rating to draw scientific conclusions. For now, the best advice is to listen to expert opinion and realize that turning our patients more frequently than not is important for pressure ulcer prevention.

References

1. Kosiak M. Etiology and pathology of ischemic ulcers. Arch Phys Med Rehabil 1959;40(2):62–9.
2. Landis E. Micro-injection studies of capillary blood pressure in human skin. Heart 1930;15:209–28.
3. Salcido R, Carney J, Fisher S. A reliable animal model of pressure sore development: the role of free radicals. J Am Paraplegia Soc 1993;16:61.
4. Salcido R, Donofrio JC, Fisher SB, et al. Histopathology of pressure ulcers as a result of sequential computer-controlled pressure sessions in a fuzzy rat model. Adv Wound Care 1994;7(5):23–4, 26, 28, passim.
5. Russ G, Motta G. Eliminating pressure: is less than 32 mm Hg enough for wound healing? Ostomy Wound Manage 1991;34:60–3.
6. Husain T. Experimental study of some pressure effects on tissues, with reference to the bed-sore problem. J Pathol Bacteriol 1953;66(2):347–58.
7. Dinsdale SM. Decubitus ulcers in swine: light and electron microscopy study of pathogenesis. Arch Phys Med Rehabil 1973;54(2):51–6 passim.
8. Reswick J, Rogers JE. Experience at Rancho Los Amigos Hospital with devices and techniques to prevent pressure ulcers. In: Kenedi R, Cowden J, Scales J, editors. Bedsore Biomechanics. London: University Park Press; 1976. p 300.
9. Reichel S. Shearing force as a factor in decubitus ulcers in paraplegics. J Am Med Assoc 1958;166(7):762–3.
© 2004 Lippincott Williams & Wilkins, Inc.