The ABA pain guidelines were developed 14 years ago and have not been revised despite evolution in the practice of burn care. A sub-committee of the American Burn Association’s Committee on the Organization and Delivery of Burn Care was created to revise the adult pain guidelines. A MEDLINE search of English-language publications from 1968 to 2018 was conducted using the keywords “burn pain,” “treatment,” and “assessment.” Selected references were also used from the greater pain literature. Studies were graded by two members of the committee using Oxford Centre for Evidence-based Medicine—Levels of Evidence. We then met as a group to determine expert consensus on a variety of topics related to treating pain in burn patients. Finally, we assessed gaps in the current knowledge and determined research questions that would aid in providing better recommendations for optimal pain management of the burn patient. The literature search produced 189 papers, 95 were found to be relevant to the assessment and treatment of burn pain. From the greater pain literature 151 references were included, totaling 246 papers being analyzed. Following this literature review, a meeting to establish expert consensus was held and 20 guidelines established in the areas of pain assessment, opioid medications, nonopioid medications, regional anesthesia, and nonpharmacologic treatments. There is increasing research on pain management modalities, but available studies are inadequate to create a true standard of care. We call for more burn specific research into modalities for burn pain control as well as research on multimodal pain control.
Introduction Severe burn injuries are known to initiate a profound systemic inflammatory response (SIRS) that may lead to burn shock and other SIRS related complications. Damage associated molecular patterns (DAMPs) are important early signaling molecules that initiate SIRS after burn injury. Mitochondrial DAMPs (mtDAMPs) – such as mitochondrial DNA (mtDNA) - are thought to be the most critical of these early signaling molecules. Previous work in a rodent model has shown that application of a topical immune modulator (p38 MAPK inhibitor) applied directly to the burn wound decreases cytokine expression, reduces pulmonary inflammation and edema and improves survival. Our group has demonstrated that tranexamic acid (TXA) – in addition to its use as an anti-fibrinolytic – has cell protective in vitro effects. We hypothesized that administration of TXA after burn injury would attenuate mtDAMP release and reduce lung inflammation. Methods C57/BL6 male mice were subjected to a 40% TBSA scald burn by immersion in an 80°C water bath. Sham animals underwent the same procedure, but were immersed in room temperature water. All animals were resuscitated according to the Parkland formula (3cc × %TBSA × Weight [Kg]) by intraperitoneal injection (IP). One treatment group received the topical application of 1mM solution of p38 MAPK inhibitor after burn injury. The other treatment group received an IP administration of TXA (100 mg TXA per 1 kg weight) after burn injury. Animals were sacrificed at 5 hours after injury or sham treatment. Plasma was collected by cardiac puncture. MtDNA levels in plasma were determined by qPCR. Syndecan-1 levels in plasma were determined by ELISA. Lungs were harvested, formalin fixed and paraffin embedded. Sections of lungs were deparaffinized and stained for Mac1 antigen to detect macrophages. Numbers of macrophages per a standard square unit of lung section were calculated. Results Topical p38 MAPK inhibitor and TXA significantly attenuated mtDNA release. Both TXA and the topical p38 MAPK inhibitor reduced lung inflammation as represented by decreased macrophage infiltration. Circulating syndecan-1 levels showed no difference between the untreated burn group and either treatment group. Conclusion Both p38 MAPK inhibitor and TXA demonstrated the ability to attenuate burn induced DAMP release and lung inflammation. Beyond its role as an anti-fibrinolytic, TXA may have significant anti-inflammatory effects pertinent to burn resuscitation. Further study is required; however, TXA may be a useful adjunct in burn resuscitation and other non-hemorrhagic shock states.
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