Nerve Pain After Burn Injury: A Proposed Etiology-based Classification
Kevin M. Klifto, PharmD, C. Scott Hultman, MD, MBA, A. Lee Dellon, MD, PhD.
The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
PURPOSE: Knowing how to manage burn-related nerve pain may be facilitated by an understanding of how pain is transmitted through peripheral nerves. This proposed classification model, based upon the etiology of nerve injury, was developed to enhance the understanding and management of nerve pain after burn injury.
METHODS: This retrospective investigation included patients' ≥15 years of age, admitted to the Burn Unit from January 1, 2014 to January 1, 2019. Nerve pain was patient-reported and clinically assessed as pain ≥6 months after burn injury, unrelated to pre-existing illnesses/medications. Nomenclature for burn-related nerve injury and pain comprised of I) direct nerve injury, II) nerve compression, III) electrical injury, and IV) nerve dysfunction secondary to systemic injury. The four nomenclature categories were individually and statistically analyzed using 52 outcome variables. Comparisons were made between each of the four categories and within each category using Fisher's exact cross-tabulation tests followed by a Bonferroni correction for all significant dichotomous variables and Kruskal-Wallis test followed by the Dunn's post-hoc test for all significant continuous variables.
RESULTS: Of the 1880 consecutive burn patients identified, 113 developed nerve pain after burn injury and were eligible for validation of the classification(direct=47, compression=12, electrical=7, systemic=47). Factors significantly associated with: I) were continuous symptoms[p<0.001], refractory nerve release response[p<0.001], nerve repair[p<0.001], and pruritus[p<0.001]; II) were positive Tinel signs[p<0.001], shooting pain[p<0.001], numbness[p=0.003], intermittent symptoms[p<0.001], increased %TBSA[p=0.019], more surgical procedures[p<0.001], SNRI use[p<0.001], opioid use[p<0.001], neuroma excision[p<0.001], nerve release[p<0.001], substance use[p=0.005], and any complication[p=0.003]; III) were positive Tinel signs[p<0.001], intermittent symptoms[p=0.002], amputations[p=0.002], fasciotomies[p<0.001], and nerve release[p<0.001]; IV) were decreased long-term pain scores[p<0.001], absence of signs and symptoms(Tinel signs[p<0.001], shooting pain[p<0.001], numbness[p<0.001], tingling[p<0.001]), pruritus[p<0.001], less of the treatments(laser[p=0.002], skin graft[p<0.001], amputation[p=0.004], nerve release[p<0.001], PT/OT[p<0.001]) and less third degree burns[p=0.002].
CONCLUSIONS: Direct nerve injury, nerve compression, electrical injury, and systemic causes of burn-related nerve pain were categorized into a classification to guide patient management and research methods, which have the potential to improve pain outcomes in this group of patients.
|I||Direct nerve injury||Excision and grafting, donor site, within burn healing by secondary intention||<0.001|
|II||Nerve compression||Occult pre-injury, internal fibrosis, external compression||<0.001|
|III||Electrical injury||Nerve in the conduction pathway of the electrical injury||<0.001|
|IV||Systemic injury||Neuromuscular weakness which develops in patients who are critically ill undergoing prolonged ventilation, acute primary axonal degeneration of sensory and motor nerve fibers and an associated degeneration of skeletal muscles||<0.001|
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