Griffis CA, Compton P, Doering L. Biological Research for Nursing. 2006;7:297-312.

REVIEWER INTRODUCTION

Two primary functions of the trauma nurse are to recognize and control pain and prevent potentially deadly complications. The information presented in this article impacts both of these actions. The authors propose an evidence-based theory stating that acute pain affects the quality of the cellular immune response to tissue injury. The quality of the immune response to trauma plays a significant role in the development of subsequent complications such as infection, sepsis, acute respiratory distress syndrome, and multiple organ dysfunction and failure.1-3 Trauma nurses can use the information in this article to change practice and improve acute outcomes of injury. The theory presented in this article can guide trauma researchers to develop future practice-based studies.

ABSTRACT

The authors begin by presenting results of relevant studies to support the individual concepts of their theory. The results are synthesized to make the following points:

1. Pain is a neurophysiological stimulus that triggers the release of chemical mediators. These mediators increase neural cell action potentials, allowing pain signals to travel along spinal pathways to activate a physiological stress response.

2. The physiological stress response to pain causes stress hormones to be released. These hormones have both pro-inflammatory and anti-inflammatory effects; however, evidence shows that the overall effect may be pro-inflammatory.

3. Pain intensity and duration influence the amount of stress hormones released, and the release of these stress hormones impacts the intensity of the overall pro-inflammatory immune response.

4. These changes may result in a positive-feedback loop in which a pro-inflammatory response results in increased pain, which, in turn, causes increased proinflammatory immune responses.

The authors summarize the research by presenting their theory, which concludes that the overall effect of the physiological changes associated with pain results in a clinically relevant exacerbation of diseases with inflammatory origins. Suggestions for further research are provided, including theory-testing studies in which the relationship of pain intensity to pro-inflammatory disease outcomes is assessed and animal studies that measure pro-inflammatory cytokines and compare them with measures of pain intensity.

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COMMENTARY

Complications of multiple injuries can be deadly. Some, such as severe sepsis, can have mortality rates as high as 80%.2 Many of these complications develop as a result of a pathological pro-inflammatory response following multiple trauma.4,5 Because treatment options for complications are limited,6 prevention is the key to improving acute outcomes of multiple trauma.7

Prevention of complications and pain control is the domain of nursing. The authors of this article provide important theoretical building blocks upon which future practice-based protocols and research can be developed. Nurse researchers can use the model to develop proposals that further describe and test relationships between adequate pain control and the subsequent development of inflammatory-related complications and associated mortality. Nurse clinicians can incorporate study results into evidence-based practice guidelines for diagnosing and treating pain caused by injury, preventing complications, and improving health outcomes for trauma patients across the care continuum.

REFERENCES