Comparative histopathological study of the phrenic nerve from corpses with chronic obstructive pulmonary disease and without this condition
Estudio histopatológico comparativo del nervio frénico proveniente de cadáveres con enfermedad pulmonar obstructiva crónica y sin esta condición
Introduction: Functional changes resulting from the evolution of chronic obstructive pulmonary disease (COPD) are progressive and irreversible, causing increased diaphragm work due to pulmonary hyperinflation and airway obstruction. Phrenic nerves have promoted innervation of the diaphragm and may have been compromised in COPD condition. Objective: To compare the morphology of the phrenic nerves of the cadavers with COPD and without COPD by optical microscopy. Materials and methods: An exploratory descriptive studio conducted on the Death Verification Service in Alagoas. Pulmonary and phrenic nerve biopsies will be bilaterally taken from the cadavers after a necropsy with the diagnosis of COPD. Tissue samples were fixed and processed by conventional histology for hematoxylin-eosin (HE) histological slides. Biopsies are divided into experimental groups, one composed by patients with COPD and the other with patients without COPD (control - CTR). This classification was realized after the histological analysis, when typical halls of COPD were found. Histological slides were analyzed by optical microscopy by a pathologist, who was able to assess the study. Results: According to the inclusion and exclusion criteria of the study, if it includes 38 cadavers in the initial evaluation, of which 31 are included in the COPD group and 7 in the CTR group. In the analysis of the phrenic nerves, 8 cadavers, 25.8%, of the COPD group had histopathological changes: perineural edema (75%, n=6), nervous atrophy (12.5%, n=1) and perineural eosinophilic infiltrate (12.5%, n=1). The CTR group does not present histopathological alterations of the phrenic nerves. Conclusions: Given the hallmarks of the biopsies performed on the phrenic nerves of the corpses with COPD, we can infer that there is a tendency for nerve alteration, with perineural edema, to be the major modification found.
2. Mathers CD, Loncar D. Projections of global mortality and burden of disease from 2002 to 2030. PLoS Med. 2006;3(11):e442.
3. Singh D, Agusti A, Anzueto A, Barnes PJ, Bourbeau J, Celli BR, et al. Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Lung Disease: the GOLD science committee report 2019. Eur Respir J. 2019;53(5).
4. Lange P, Celli B, Agustí A, Boje Jensen G, Divo M, Faner R, et al. Lung-Function Trajectories Leading to Chronic Obstructive Pulmonary Disease. N Engl J Med. 2015;373(2):111-22.
5. Alter A, Aboussouan LS, Mireles-Cabodevila E. Neuromuscular weakness in chronic obstructive pulmonary disease: chest wall, diaphragm, and peripheral muscle contributions. Curr Opin Pulm Med. 2017;23(2):129-38.
6. Negewo NA, Gibson PG, McDonald VM. COPD and its comorbidities: Impact, measurement and mechanisms. Respirology. 2015;20(8):1160-71.
7. Naruse M, Ishizaki Y, Ikenaka K, Tanaka A, Hitoshi S. Origin of oligodendrocytes in mammalian forebrains: a revised perspective. J Physiol Sci. 2017;67(1):63-70.
8. Bacci A, Verderio C, Pravettoni E, Matteoli M. The role of glial cells in synaptic function. Philos Trans R Soc Lond B Biol Sci. 1999;354(1381):403-9.
9. Ramírez-Sarmiento A, Orozco-Levi M, Barreiro E, Méndez R, Ferrer A, Broquetas J, et al. Expiratory muscle endurance in chronic obstructive pulmonary disease. Thorax. 2002;57(2):132-6.
10. Garara B, Wood A, Marcus HJ, Tsang K, Wilson MH, Khan M. Intramuscular diaphragmatic stimulation for patients with traumatic high cervical injuries and ventilator dependent respiratory failure: A systematic review of safety and effectiveness. Injury. 2016;47(3):539-44.
11. Martinelli LM, Boas PJ, Queluz TT, Yoo HH. Morphological prognostic factors in nosocomial pneumonia: an autopsy study. J Bras Pneumol. 2010;36(1):51-8.
12. Churg A, Brauer M, del Carmen Avila-Casado M, Fortoul TI, Wright JL. Chronic exposure to high levels of particulate air pollution and small airway remodeling. Environ Health Perspect. 2003;111(5):714-8.
13. Lagente V, Manoury B, Nénan S, Le Quément C, Martin-Chouly C, Boichot E. Role of matrix metalloproteinases in the development of airway inflammation and remodeling. Braz J Med Biol Res. 2005;38(10):1521-30.
14. Nations SP, Katz JS, Lyde CB, Barohn RJ. Leprous neuropathy: an American perspective. Semin Neurol. 1998;18(1):113-24.
15. Antia NH. The significance of nerve involvement in leprosy. Plast Reconstr Surg. 1974;54(1):55-63.
16. Walker SL, Lockwood DN. Leprosy type 1 (reversal) reactions and their management. Lepr Rev. 2008;79(4):372-86.
17. Forgione P, Barabino G, Cavalchini A, Clapasson A, Reni L, Parodi A. Pure neuritic leprosy. G Ital Dermatol Venereol. 2018;153(1):124-6.
18. Scott A, Wang X, Road JD, Reid WD. Increased injury and intramuscular collagen of the diaphragm in COPD: autopsy observations. Eur Respir J. 2006;27(1):51-9.
19. Orozco-Levi M. Structure and function of the respiratory muscles in patients with COPD: impairment or adaptation? Eur Respir J Suppl. 2003;46:41s-51s.
20. Levine S, Gregory C, Nguyen T, Shrager J, Kaiser L, Rubinstein N, et al. Bioenergetic adaptation of individual human diaphragmatic myofibers to severe COPD. J Appl Physiol (1985). 2002;92(3):1205-13.
21. DiMarco AF. Diaphragm Pacing. Clin Chest Med. 2018;39(2):459-71.
22. Proctor DN, Balagopal P, Nair KS. Age-related sarcopenia in humans is associated with reduced synthetic rates of specific muscle proteins. J Nutr. 1998;128(2 Suppl):351S-5S.
This work is under a Creative Commons license Attribution 4.0 International (CC BY 4.0).