Patofisiologi Acute Mountain Sickness
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Abstract
Pendahuluan: Acute mountain sickness (AMS) adalah kelainan neurologis yang biasanya menyerang pendaki gunung yang berada di ketinggian akibat hipoksia kronis pada tekanan parsial oksigen rendah. Walaupun seringkali bersifat self-limiting, AMS dapat menyebabkan edema pulmonal dan serebral yang dapat bersifat fatal. Popularitas pendakian gunung yang meningkat dan mudahnya akses beberapa tahun terakhir menyebabkan peningkatan jumlah pendaki yang berisiko mengalami bahaya AMS.
Pembahasan: Rendahnya tekanan oksigen pada ketinggian akan memicu 4 mekanisme refleks: respons ventilasi hipoksia, respons ventilasi hiperkapnia, vasodilatasi pembuluh otak terhadap hipoksia, dan vasokonstriksi pembuluh darah otak terhadap hipokapnia. Kejadian ini akan memicu pembengkakan astrosit dan aktivasi sistem trigeminovaskular sehingga menyebabkan gejala neurologis pendaki.
Kesimpulan: Pada keadaan di ketinggian, terjadi penurunan tekanan parsial O2 sehingga menyebabkan terjadinya hipoksemia pada pendaki. Kegagalan autoregulasi aliran darah otak akan menyebabkan peningkatan tekanan kranial melalui gaya mekanik dan kebocoran kapiler melalui gaya kimia. Hipertensi intrakranial akan menyebabkan perpindahan dan peregangan serabut saraf sensitif yang tidak termielinisasi pada sistem trigeminovaskular sehingga menyebabkan gejala neurologis pendaki.
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References
2. Bailey D, Bartsch P, Knauth M. Emerging concepts in acute mountain sickness and high-altitude cerebral edema: from the molecular to the morphological. Cell Mol Life Sci. 2009; 66:3583-8
3. Clarke C. Acute mountain sickness: medical problems associated with acute and subacute exposure to hypobaric hypoxia. Postgrad Med J. 2006; 82(973):748-53
4. Sherwood L. Human physiology. 9th ed. Boston: Cengage Learning; 2016. p. 445
5. Guyton AC, Hall JE. Guyton and hall textbook of medical physiology. 13th ed. Philadelphia: Elsevier, Inc.; 2013. p. 539
6. Elvira D. High-altitude illnes. JKA. 2015; 4(2):582-5
7. Brown J, Grocott M. Humans at altitude: physiology and pathophysiology. Brit J Ans. 2013; 3:20
8. Severinghaus JW. Cerebral circulation at altitude. 2nd ed. New York: Elsevier; 2001. pp. 343–375.
9. Ainslie P, Subudhi A. Cerebral blood flow at high altitude. High Al Med Biol. 2014;15(2):137-8
10. Ainslie P, Wilson M, and Imray C. Cerebral circulation at brain. New York: Springer. 2014. pp. 135-7
11. Sanchez del Rio M, Moskowitz M. High altitude headache: Lessons from headaches at sea level. Adv Exp Med Biol. 1999; 474:145–53
12. Kallenberg K, Bailey DM, Christ S, Mohr A, Roukens R, Menold E, Steiner T, Bartsch P, Knauth M. Magnetic resonance imaging evidence of cytotoxic cerebral edema in acute mountain sickness. J Cereb Blood Flow Metab. 2007; 27:1064–71
13. Goadsby P, Lipton R, Ferrari M. Migraine-current under- standing and treatment. N Engl J Med. 2002; 346:257–8
14. Hildebrandt W, Alexander S, Bartsch P, Droge W. Effect of N-acetyl-cysteine on the hypoxic ventilatory response and erythropoietin production: linkage between plasma thiol redox state and O2 chemosensitivity. Blood. 2002; 99:1552–5
15. Wilkins M, Ghofrani H, Weissmann N. Pathophysiology and treatment of high pulmonary vascular disease. Cir AHA J. 2015; 131:582-3
16. Sylvester JT, Shimoda LA, Aaronson PI, Ward JP. Hypoxic pulmonary vasoconstriction. Physiol Rev. 2012;92:367. doi: 10.1152/ physrev.00041.2010.
17. Schwenke DO, Pearson JT, Umetani K, Kangawa K, Shirai M. Imaging of the pulmonary circulation in the closed-chest rat using synchrotron radiation microangiography. J Appl Physiol (1985). 2007;102:787–93. doi: 10.1152/japplphysiol.00596.2006.
18. Swenson ER. Hypoxic pulmonary vasoconstriction. High Alt Med Biol. 2013;14:101–110. doi: 10.1089/ham.2013.1010.
19. Wang L, Yin J, Nickles T, Ranke H, Tabuchi A. Hypoxic pulmonary vasoconstriction requires connexin 40-mediated endothelial signal conduction. J Clin Invest. 2012;122:4218–9. doi: 10.1172/JCI59176.
20. Murray T, Chen L, Marshall B, Macarak E. Hypoxic contraction of cultured pulmonary vascular smooth muscle cells. Am J Respir Cell Mol Biol. 1990;3:457. doi: 10.1165/ajrcmb/3.5.457.
21. Wiener C, Sylvester J. Effects of glucose on hypoxic vasoconstriction in isolated ferret lungs. J Appl Physiol (1985). 1991;70:439–446.
22. Kim YM, Barnes EA, Alvira CM, Ying L, Reddy S, Corn eld DN. Hypoxia-inducible factor-1 in pulmonary artery smooth muscle cells lowers vascular tone by decreasing myosin light chain phosphorylation. Circ Res. 2013;112:1230–1233. doi: 10.1161/CIRCRESAHA.112.300646