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A Case of Acute Type A Aortic Dissection Complicated with High-Altitude Pulmonary Edema

Received: 26 November 2023    Accepted: 13 December 2023    Published: 26 December 2023
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Abstract

We report a case of a 55-year-old middle-aged male patient who developed dyspnea while traveling in a high-altitude region. After further investigations, he was diagnosed with high-altitude pulmonary edema (HAPE). During the treatment process, he was urgently transferred to our hospital due to chest pain, and a computed tomography angiography (CTA) confirmed acute type A aortic dissection (ATAAD). The patient underwent an emergency Bentall procedure, total arch replacement, and descending aortic stent placement. The surgery was uneventful. The postoperative recovery was smooth and the patient was discharged in good condition. ATAAD is a critical condition in cardiac surgery, with a low incidence rate but an increasing trend. It is associated with high mortality rates. Acute pulmonary edema is one of the complications of aortic dissection, possibly related to acute aortic valve insufficiency and the release of inflammatory factors leading to pulmonary capillary damage. Acute pulmonary edema will seriously affect lung function, and the resulting hypoxemia will also lead to hypoxia in tissue cells of organs throughout the body, leading to disorder of the body's internal environment. HAPE refers to the patient who has recently arrived at a plateau (generally above 3,000 meters above sea level) and has difficulty breathing at rest, chest tightness, cough, white or pink foamy sputum, and the patient feels general weakness or reduced mobility. The main pathological change of high-altitude pulmonary edema is extensive alveolar edema distributed in patches, and occasionally the formation of hyaline membranes can be seen (this is caused by fibrin deposition in the alveolar edema fluid). HAPE is a non-cardiogenic pulmonary edema specific to high-altitude regions, with severe conditions and high mortality rates. The current understanding suggests that the mechanism of HAPE involves excessive elevation of pulmonary arterial pressure due to hypoxia, increased pulmonary vascular permeability, impaired pulmonary fluid clearance, fluid retention, and fluid transport imbalance. Acute pulmonary edema is a relatively rare presentation of aortic dissection, and the combination of ATAAD and HAPE is extremely rare, posing additional challenges to surgical treatment and anesthesia management.

Published in Cardiology and Cardiovascular Research (Volume 7, Issue 4)
DOI 10.11648/j.ccr.20230704.16
Page(s) 97-100
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2024. Published by Science Publishing Group

Keywords

Acute Type A Aortic Dissection, High-Altitude Pulmonary Edema, Acute Pulmonary Edema

References
[1] Apostolakis E, Akinosoglou K. What' s new in the biochemical diagnosis of acute aortic dissection dissection: Problems and perspectives [J]. Med Sci Monit, 2007, 13(8): RA154-158.
[2] Bekeredjian R, Grayburn PA. Valvular heart disease: aortic regurgitation. Circulation. 2005 Jul 5; 112(1): 125-34. doi: 10.1161/CIRCULATIONAHA.104.488825.
[3] Clouse WD, Hallett JW, Schaf HV, et al. Acute aortic dissection: population-based incidence compared with degenerative aortic aneurysm rupture. Mayo Clin Proc. 2004 Feb; 79(2): 176-80. doi: 10.4065/79.2.176.
[4] Melvinsdottir IH, Lund SH, Agnarsson BA, et al. The incidence and mortality of acute thoracic aortic dissection: results from a whole nation study. Eur J Cardiothorac Surg. 2016 Dec; 50(6): 1111-1117. doi: 10.1093/ejcts/ezw235.
[5] Hagan PG, Nienaber CA, Isselbacher EM, et al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA. 2000 Feb 16; 283(7): 897-903. doi: 10.1001/jama.283.7.897.
[6] Siddiqui WJ, Arif A, Khan MH, Khan M, et al. An Atypical Case of Silent Aortic Dissection in a Peritoneal Dialysis Patient: A Case Report and Review of Literature. Am J Case Rep. 2018 Jul 27: 19: 880-883. doi: 10.12659/AJCR.909966.
[7] Ohle R, Kareemi HK, Wells G, Perry JJ. Clinical Examination for Acute Aortic Dissection: A Systematic Review and Meta-analysis. Acad Emerg Med. 2018 Apr; 25(4): 397-412. doi: 10.1111/acem.13360.
[8] Khan IA, Nair CK. Clinical, diagnostic, and management perspectives of aortic dissection. Chest. 2002 Jul; 122(1): 311-28. doi: 10.1378/chest.122.1.311.
[9] Mussa FF, Horton JD, Moridzadeh R, Nicholson J, Trimarchi S, Eagle KA. Acute Aortic Dissection and Intramural Hematoma: A Systematic Review. JAMA. 2016 Aug 16; 316(7): 754-63. doi: 10.1001/jama.2016.10026.
[10] Lien WC, Wang CH, Chang WT, Hsu RB, Chen WJ. Aortic dissection presenting with acute pulmonary edema. Am J Emerg Med. 2018 Jul; 36(7): 1323. e7-1323. e9. doi: 10.1016/j.ajem.2018.04.001. Epub 2018 Apr 3.
[11] Pei C, Jia N, Wang Y, Zhao S, et al. Notoginsenoside R1 protects against hypobaric hypoxia-induced high-altitude pulmonary edema by inhibiting apoptosis via ERK1/2-P90rsk-BAD ignaling pathway. Eur J Pharmacol. 2023 Nov 15: 959: 176065. doi: 10.1016/j.ejphar.2023.176065. Epub 2023 Sep 27.
[12] Khan M, Bordes SJ, Murray IV, Sharma S. Physiology, Pulmonary Vasoconstriction. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan. 2023 Apr 17.
[13] Gojkovic M, Darmasaputra GS., Veliça P, Rundqvist H, et al. Deregulated hypoxic response in myeloid cells: A model for high-altitude pulmonary oedema (HAPE). Acta Physiol (Oxf) 2020 Jun; 229(2): e13461. doi: 10.1111/apha.13461. Epub 2020 Mar 16.
[14] Zong HF, Guo G, Liu J, Yang, CZ, et al. Influence of alveolar fluid on aquaporins and Na+/K+-ATPase and its possible theoretical or clinical significance [J]. Am J Perinatol. 2022 Oct; 29(14): 1586-1595. doi: 10.1055/s-0041-1724001. Epub 2021 Feb 21.
[15] Hudalla H, Michael Z, Christodoulou N, Willis G, et al. Carbonic Anhydrase Inhibition Ameliorates Inflammation and Experimental Pulmonary Hypertension [J]. Am J Respir Cell Mol Biol. 2019 Oct; 61(4): 512-524. doi: 10.1165/rcmb.2018-0232OC.
[16] Oz K, Iyigun T, Karaman Z, et al. Prognostic value of neutrophil to lymphocyte ratio and risk factors for mortality in patients with Stanford type A aortic dissection. Heart Surg Forum. 2017 Jun 30; 20(3): E119-E123. doi: 10.1532/hsf.1736.
[17] Koerner MM, Loebe M, Lisman KA, et al. New strategies for the management of acute decompensated heart failure. Curr Opin Cardiol. 2001 May; 16(3): 164-73. doi: 10.1097/00001573-200105000-00002.
Cite This Article
  • APA Style

    Song, L., Li, X. (2023). A Case of Acute Type A Aortic Dissection Complicated with High-Altitude Pulmonary Edema. Cardiology and Cardiovascular Research, 7(4), 97-100. https://doi.org/10.11648/j.ccr.20230704.16

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    ACS Style

    Song, L.; Li, X. A Case of Acute Type A Aortic Dissection Complicated with High-Altitude Pulmonary Edema. Cardiol. Cardiovasc. Res. 2023, 7(4), 97-100. doi: 10.11648/j.ccr.20230704.16

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    AMA Style

    Song L, Li X. A Case of Acute Type A Aortic Dissection Complicated with High-Altitude Pulmonary Edema. Cardiol Cardiovasc Res. 2023;7(4):97-100. doi: 10.11648/j.ccr.20230704.16

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  • @article{10.11648/j.ccr.20230704.16,
      author = {Lin Song and Xuejie Li},
      title = {A Case of Acute Type A Aortic Dissection Complicated with High-Altitude Pulmonary Edema},
      journal = {Cardiology and Cardiovascular Research},
      volume = {7},
      number = {4},
      pages = {97-100},
      doi = {10.11648/j.ccr.20230704.16},
      url = {https://doi.org/10.11648/j.ccr.20230704.16},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ccr.20230704.16},
      abstract = {We report a case of a 55-year-old middle-aged male patient who developed dyspnea while traveling in a high-altitude region. After further investigations, he was diagnosed with high-altitude pulmonary edema (HAPE). During the treatment process, he was urgently transferred to our hospital due to chest pain, and a computed tomography angiography (CTA) confirmed acute type A aortic dissection (ATAAD). The patient underwent an emergency Bentall procedure, total arch replacement, and descending aortic stent placement. The surgery was uneventful. The postoperative recovery was smooth and the patient was discharged in good condition. ATAAD is a critical condition in cardiac surgery, with a low incidence rate but an increasing trend. It is associated with high mortality rates. Acute pulmonary edema is one of the complications of aortic dissection, possibly related to acute aortic valve insufficiency and the release of inflammatory factors leading to pulmonary capillary damage. Acute pulmonary edema will seriously affect lung function, and the resulting hypoxemia will also lead to hypoxia in tissue cells of organs throughout the body, leading to disorder of the body's internal environment. HAPE refers to the patient who has recently arrived at a plateau (generally above 3,000 meters above sea level) and has difficulty breathing at rest, chest tightness, cough, white or pink foamy sputum, and the patient feels general weakness or reduced mobility. The main pathological change of high-altitude pulmonary edema is extensive alveolar edema distributed in patches, and occasionally the formation of hyaline membranes can be seen (this is caused by fibrin deposition in the alveolar edema fluid). HAPE is a non-cardiogenic pulmonary edema specific to high-altitude regions, with severe conditions and high mortality rates. The current understanding suggests that the mechanism of HAPE involves excessive elevation of pulmonary arterial pressure due to hypoxia, increased pulmonary vascular permeability, impaired pulmonary fluid clearance, fluid retention, and fluid transport imbalance. Acute pulmonary edema is a relatively rare presentation of aortic dissection, and the combination of ATAAD and HAPE is extremely rare, posing additional challenges to surgical treatment and anesthesia management.
    },
     year = {2023}
    }
    

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  • TY  - JOUR
    T1  - A Case of Acute Type A Aortic Dissection Complicated with High-Altitude Pulmonary Edema
    AU  - Lin Song
    AU  - Xuejie Li
    Y1  - 2023/12/26
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    JO  - Cardiology and Cardiovascular Research
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    AB  - We report a case of a 55-year-old middle-aged male patient who developed dyspnea while traveling in a high-altitude region. After further investigations, he was diagnosed with high-altitude pulmonary edema (HAPE). During the treatment process, he was urgently transferred to our hospital due to chest pain, and a computed tomography angiography (CTA) confirmed acute type A aortic dissection (ATAAD). The patient underwent an emergency Bentall procedure, total arch replacement, and descending aortic stent placement. The surgery was uneventful. The postoperative recovery was smooth and the patient was discharged in good condition. ATAAD is a critical condition in cardiac surgery, with a low incidence rate but an increasing trend. It is associated with high mortality rates. Acute pulmonary edema is one of the complications of aortic dissection, possibly related to acute aortic valve insufficiency and the release of inflammatory factors leading to pulmonary capillary damage. Acute pulmonary edema will seriously affect lung function, and the resulting hypoxemia will also lead to hypoxia in tissue cells of organs throughout the body, leading to disorder of the body's internal environment. HAPE refers to the patient who has recently arrived at a plateau (generally above 3,000 meters above sea level) and has difficulty breathing at rest, chest tightness, cough, white or pink foamy sputum, and the patient feels general weakness or reduced mobility. The main pathological change of high-altitude pulmonary edema is extensive alveolar edema distributed in patches, and occasionally the formation of hyaline membranes can be seen (this is caused by fibrin deposition in the alveolar edema fluid). HAPE is a non-cardiogenic pulmonary edema specific to high-altitude regions, with severe conditions and high mortality rates. The current understanding suggests that the mechanism of HAPE involves excessive elevation of pulmonary arterial pressure due to hypoxia, increased pulmonary vascular permeability, impaired pulmonary fluid clearance, fluid retention, and fluid transport imbalance. Acute pulmonary edema is a relatively rare presentation of aortic dissection, and the combination of ATAAD and HAPE is extremely rare, posing additional challenges to surgical treatment and anesthesia management.
    
    VL  - 7
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Author Information
  • Department of Anesthesiology, West China Hospital, Sichuan University and the Research Units of West China (2018RU012), Chinese Academy of Medical Sciences, Chengdu, China

  • Department of Anesthesiology, West China Hospital, Sichuan University and the Research Units of West China (2018RU012), Chinese Academy of Medical Sciences, Chengdu, China

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