Pulmonary Histopathological Findings Following Recurrent Laryngeal Nerve Injury and Reconstruction in Rats: An Experimental Study

Abstract Recurrent laryngeal nerve (RLN) injury causes vocal fold paralysis and increases aspiration risk, but the downstream pulmonary histopathological consequences of different repair strategies remain unexplored. In this secondary analysis of tissue from a parent experiment, we compared lung changes after experimental RLN transection among three groups of rats (n = 9/group): unrepaired control, primary end-to-end neurorrhaphy, and neurorrhaphy augmented with donor-derived fibrin matrix. Lungs were harvested at approximately 3 months and nine semi-quantitative parameters were combined into total, parenchymal, and inflammatory injury scores. The total lung injury score differed among groups (P = .003): it was higher after primary repair (median 11.0) than after no repair (8.0; P = .004) or fibrin-augmented repair (8.0; P = .023). Parenchymal injury was higher after primary repair than after no repair, and inflammatory injury was higher after primary repair than after fibrin-augmented repair; pulmonary edema and parenchymal inflammation were the only individual parameters that differed, and bronchial diameter did not. Vocal fold muscle atrophy correlated with the inflammatory score (rho = 0.401, P = .038; exploratory). These findings are hypothesis-generating: the study was not powered for pulmonary outcomes, and whether fibrin-matrix augmentation limits distant pulmonary sequelae requires confirmation in adequately powered studies.