High Altitude Pulmonary Edema Research Articles

High altitude exercise stress echocardiograph for identification of susceptibility to acute mountain sickness

Abstract Background Acute high-altitude exposure increases the risk of acute mountain disease (AMS) and high-altitude pulmonary edema. After the initial exposure to high altitude, mountain climbers are worried about whether they will develop AMS. At high altitudes, there are no accurate indicators to predict the near future occurrence of AMS. Objectives To investigate whether treadmill exercise stress echocardiography at high altitude can predict the occurrence of AMS, and to find out some powerful factors associated with the susceptibility to AMS. Methods 36 healthy lowlanders were taken by bus from sea level to an altitude of 3600 m the next morning, during which they rested overnight at an altitude of 2150 m. Treadmill exercise stress echocardiography was performed immediately upon arrival at 2150 m, and the 2018 Lake Louise Questionnaire Score was performed the next day when arrived at the altitude of 3600 m. Heart rate (HR) and blood pressure (BP) were monitored during stress echocardiography. Left ventricular (LV) ejection fraction and E/e’ were calculated at rest and immediately after exercise. Other right ventricular systolic function parameters and pulmonary artery pressure (PAP) were calculated at the same time, which included tricuspid regurgitation velocity (TRV), tricuspid annular peak systolic excursion (TAPSE), systolic PAP (SPAP), right ventricular (RV) dimension by 2D, RV fraction of area change (FAC), right ventricular outflow tract velocity time integral (RVOT VTI). Pulmonary vascular resistance (PVR) was calculated according to the formula: TRV/RVOT VTI*10+0.16. Mean PAP (mPAP) was calculated as the formula: sPAP*0.61+2. All subjects ascended to 3600m within 24 hours by bus. AMS was identified by 2018 Lake Louise Questionnaire Score. Univariable and multivariable logistic regression analysis assessed independent factors associated with AMS. Results At the altitude of 3600m, 13 of 36 subjects had AMS, which defined as AMS (+) group. And the rest was AMS (-) group. There were no significant differences in HR, BP, SO2 and LV systolic and diastolic function between the two groups (P > 0.05). No significant differences were noted at rest except for TV s' (P < 0.05). Immediately after exercise, TRV, TAPSE, SPAP, mPAP, PVR, and RV area at the end of systole were much higher in AMS (+) group (all P < 0.05). While FAC and TVs’/SPAP were much lower in AMS (+) group (P < 0.05). By multivariable logistic regression model, mPAP immediately after exercise was significantly correlated with AMS occurrence (OR =1.332, 95% CI: 0.669-0.993, P= 003). The cutoff value of mPAP to predict AMS was 32 mmHg (AUC: 0.831, specificity: 86.7%, sensitivity: 76.9%). Conclusions The mPAP immediately after exercise upon arrival at an altitude of 2150 m is a strong predictor of near future AMS, and treadmill exercise stress echocardiography is a simple and non-invasive tool to help mountain climbers avoid more severe mountain sickness.

Impact of MIR137HGrs7554283 on susceptibility to high-altitude pulmonary edema in the Chinese population.

Aim: MIR137 host gene (MIR137HG) variants were involved in a variety of diseases, but its role in high-altitude pulmonary edema (HAPE) has not been reported. The study aimed to study the association between MIR137HG single-nucleotide polymorphisms and HAPE risk in the Chinese population.Materials & methods: Based on the Plink software, odds ratio and 95% confidence interval were used for logistic regression analysis to evaluate the association between MIR137HG polymorphisms and the risk of HAPE.Results: We discovered that MIR137HG rs7554283 was associated with a reduced risk of HAPE. In both individuals older than 32years and those younger than 32years, we observed that rs7554283 was associated with a decreased risk of HAPE.Conclusion: In conclusion, MIR137HG rs7554283 may be related to a reduced susceptibility to HAPE in the Chinese population. These results provide a theoretical basis for the role of MIR137HG single-nucleotide polymorphisms in the occurrence of HAPE.

Lung function and blood gas of rats after different protocols of hypobaric exposure.

High-altitude pulmonary edema (HAPE) is a common disease observed in climbers, skiers and soldiers who ascend to high altitudes without previous acclimatization. Thus, a reliable and reproducible animal model that can mimic the mechanisms of pathophysiologic response in humans is crucial for successful investigations. Our results showed that exposure to 4500 m for 2 days had little influence on lung function or blood gas, and exposure to 6000 m for 2 or 3 days could change lung function and blood gas, but most parameters returned to nearly normal levels within 48 hours. This study indicates that exposure to 6000 m for 3 days may induce evident lung edema and significantly alter lung function and blood gas, which may mimic HAPE in clinical practice. Thus, this animal model of HAPE may be used in future studies on HAPE.

112 High Altitude Pulmonary Edema Response to Continuous Airway Positive Pressure: The HAPER CAPER Trial

112 High Altitude Pulmonary Edema Response to Continuous Airway Positive Pressure: The HAPER CAPER Trial

Pre-treatment with notoginsenoside R1 from Panax notoginseng protects against high-altitude-induced pulmonary edema by inhibiting pyroptosis through the NLRP3/caspase-1/GSDMD pathway

High-altitude pulmonary edema (HAPE) is a potentially fatal condition that occurs when exposed to high-altitude hypoxia environments. Currently, there is no effective treatment for HAPE, and available interventions focus on providing relief. Notoginsenoside R1 (NGR1), a major active constituent of Panax notoginseng (Burkill) F.H.Chen (sānqī), has demonstrated heart and lung-protective effects under hypobaric hypoxia. However, there is a lack of clarity regarding the precise mechanisms that underlie the protective effects of NGR1 against inflammation.In this study, a rat model of HAPE was developed to assess the effect of NGR1 on this pathology. High-altitude hypoxia corresponding to 6000m altitude was simulated with a hypobaric chamber. We found that NGR1 dose-dependently alleviated pulmonary oxidative stress damage and inflammatory response, and prevented acid-base balance disruption. In addition, NGR1 restored the expression levels of hypoxia-inducible factor-1 alpha, vascular endothelial growth factor, and aquaporin protein-5, correlated with the development of pulmonary edema induced by hypobaric hypoxia. Furthermore, NGR1 pre-treatment remarkably mitigated NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome-induced pyroptosis, and this effect was partially counteracted by the use of an NLRP3 agonist. Thus, NGR1 may exert a lung-protective effect against HAPE by ameliorating hypoxia-induced lung edema, oxidative damage, and inflammation through inhibition of the NLRP3/Caspase-1/ GSDMD signaling pathway.

Physiopathology of High-Altitude Pulmonary Edema.

The air-blood barrier is well designed to accomplish the matching of gas diffusion with blood flow. This function is achieved by maintaining its thickness at ∼0.5 µm, a feature implying to keep extravascular lung water to the minimum. Exposure to hypobaric hypoxia, especially when associated with exercise, is a condition potentially leading to the development of the so-called high-altitude pulmonary edema (HAPE). This article presents a view of the physiopathology of HAPE by merging available data in humans exposed to high altitude with data from animal experimental approaches. A model is also presented to characterize HAPE nonsusceptible versus susceptible individuals based on the efficiency of alveolar-capillary oxygen uptake and estimated morphology of the air-blood barrier.

Clinical and Pathophysiological Features of High-altitude Pulmonary Edema in the Japanese Population: A Review of Studies on High-altitude Pulmonary Edema in Japan.

High-altitude pulmonary edema (HAPE) is a life-threatening, noncardiogenic pulmonary edema that occurs in unacclimatized individuals rapidly ascending to high altitudes above 2,500 m above sea level. Until the entity of HAPE was first identified in a case report published in Japan in 1966, the symptoms of severe dyspnea or coma occurring in climbers of the Japan Alps were incorrectly attributed to pneumonia or congestive heart failure. The Shinshu University Hospital serves as the central facility for rescuing and treating patients with HAPE in the region. Over the past 50 years, a series of studies have been conducted at Shinshu University to gain a better understanding of the characteristics of HAPE. This review summarizes the major achievements of these studies, including their clinical features, management, and pathogenesis of HAPE, particularly in the Japanese population.

Identification and Validation of STC1 Act as a Biomarker for High-Altitude Diseases and Its Pan-Cancer Analysis.

High-altitude diseases, including acute mountain sickness (AMS), high-altitude cerebral edema (HACE), and high-altitude pulmonary edema (HAPE), are closely related to an individual's ability to adapt to hypoxic environments. However, specific research in this field is relatively limited, and further biomarker research and clinical trials are needed to clarify the exact role and potential therapeutic applications of key genes in high-altitude diseases. This study focuses on the role of the STC1 gene in high-altitude diseases and explores its expression patterns in different types of cancer. By using gene expression data analysis and functional experiments, we identified STC1 as a key gene affecting the development of altitude sickness. In addition, we also conducted expression and mutation analysis on STC1 in various cancer samples and found significant differences in the expression of this gene in 13 types of malignant tumors, which is associated with the hypoxic state in the tumor microenvironment. In addition, STC1 is significantly associated with patient prognosis and influences tumor immunity by mediating six types of immune cells (CD8+T cells, CD4+T cells, neutrophils, macrophages, monocytes, and B cells) in the tumor microenvironment. The expression and diagnostic value of STC1 were confirmed through GEO datasets and qPCR testing, indicating consistency with the results of bioinformatics analysis. These results indicate that STC1 is not only an important factor in the adaptive response to high-altitude diseases but may also play a role in the adaptation of cancer to low-oxygen environments. Our research provides a new perspective and potential targets for the discovery of biomarkers for high-altitude diseases and cancer treatment.

TNF-α and RPLP0 drive the apoptosis of endothelial cells and increase susceptibility to high-altitude pulmonary edema

High-altitude pulmonary edema (HAPE) is a fatal threat for sojourners who ascend rapidly without sufficient acclimatization. Acclimatized sojourners and adapted natives are both insensitive to HAPE but have different physiological traits and molecular bases. In this study, based on GSE52209, the gene expression profiles of HAPE patients were compared with those of acclimatized sojourners and adapted natives, with the common and divergent differentially expressed genes (DEGs) and their hub genes identified, respectively. Bioinformatic methodologies for functional enrichment analysis, immune infiltration, diagnostic model construction, competing endogenous RNA (ceRNA) analysis and drug prediction were performed to detect potential biological functions and molecular mechanisms. Next, an array of in vivo experiments in a HAPE rat model and in vitro experiments in HUVECs were conducted to verify the results of the bioinformatic analysis. The enriched pathways of DEGs and immune landscapes for HAPE were significantly different between sojourners and natives, and the common DEGs were enriched mainly in the pathways of development and immunity. Nomograms revealed that the upregulation of TNF-α and downregulation of RPLP0 exhibited high diagnostic efficiency for HAPE in both sojourners and natives, which was further validated in the HAPE rat model. The addition of TNF-α and RPLP0 knockdown activated apoptosis signaling in endothelial cells (ECs) and enhanced endothelial permeability. In conclusion, TNF-α and RPLP0 are shared biomarkers and molecular bases for HAPE susceptibility during the acclimatization/adaptation/maladaptation processes in sojourners and natives, inspiring new ideas for predicting and treating HAPE.

Recent Progress in the Understanding and Management of Acute Mountain Sickness: A Narrative Review.

Individuals at higher altitudes may experience a decrease in blood oxygen levels, which can result in a variety of clinical illnesses, such as high-altitude pulmonary edema, high-altitude cerebral edema, and milder but more common acute mountain sickness (AMS). This study aims to review the current state of knowledge related to motion sickness, the risk of AMS, and pharmacological and non-pharmacological treatments for AMS. Several databases, including PubMed, Bentham Science, Elsevier, Springer, and Research Gate, were used to compile the data for the article following a thorough analysis of the various research findings connected to acute mountain sickness and motion sickness, along with treatments and prevention. This article covers the research on mountain sickness as well as every imaginable form of conventional and alternative medicine. It contains ten medicinal plants that are useful in treating mountain sickness and various other remedies. Additionally, case studies are provided. Therefore, the information in the paper will help travel medicine specialists better personalize their appropriate care for patients who travel to high-altitude locations. Additionally, all available antiemetic medications, serotonin agonists, nonsteroidal anti-inflammatory drugs, and herbal treatments for motion sickness were discussed. The prevention and consequences of acute mountain sickness are also covered in this study.

Corrigendum to: B2M is a Biomarker Associated With Immune Infiltration In High Altitude Pulmonary Edema.

The funding details have been incorporated upon author's request in the funding section of this article titled "B2M is a Biomarker Associated With Immune Infiltration In High Altitude Pulmonary Edema ," 2024, 27(1), 168-185 [1]. Details of the error and a correction are provided here. Original: This work was supported by grants from the Chongqing Natural Science Gene General Project (No. YWRYPYG). Corrected: This work was supported by General Project of Chongqing Natural Science Foundation cstc2020jcyj-msxmX0227. We regret the error and apologize to the readers. The original article can be found online at www.eurekaselect.com/article/131669.

Reversible leukoencephalopathy with seizures: a case of severe high-altitude cerebral edema

BackgroundAcute high-altitude illness (AHAI) refers to a series of syndromes including acute mountain sickness (AMS), high-altitude pulmonary edema (HAPE) and high-altitude cerebral edema (HACE). Among these, HACE is a severe and potentially life-threatening condition that can occur when individuals ascend to high altitudes. It is often characterized by ataxia, confusion, and altered mental status. Without appropriate treatment, HACE can rapidly progress to coma, but seizures are infrequent in occurrence.Case presentationHere, we report a severe HACE patient with coma and status epilepticus. The patient is a 23-year-old male who was visiting Lhasa for the first time. He initially experienced headaches and dizziness on the first day, and then he was found in coma with limb convulsions on the next day. Immediate medical attention was sought, and brain CT and MRI scans showed reversible white matter lesions, especially in the corpus callosum and subcortical white matter. Although the lesions disappeared on T1 and T2 sequences, microbleeds were observed on the SWI sequence. After treatment with tracheal intubation, glucocorticoids and hyperbaric oxygen, the cerebral edema has resolved and the clinical symptoms improved, the patient has no seizures anymore.ConclusionsHACE typically follows AMS and poses a significant risk to life. Clinical manifestations mainly include ataxia, alterations of behavior, and impaired consciousness, with severe cases progressing to coma. Seizures, though rarely observed, may occur. Imaging shows reversible white matter lesions, with microbleeds being a significant and persistent imaging marker over time. Administration of glucocorticoids plays a crucial role in treatment. Despite experiencing seizures, this patient did not experienced any further episodes once his condition improved.

Cardiovascular effects of breath-hold diving at altitude

ABSTRACT Marabotti C, Laurino M, Passera M, Cialoni D, Franzino E, Benvenuti C, Pingitore A. Cardiovascular effects of breath-hold diving at altitude. Undersea Hyperb Med. 2024 Second Quarter; 51(2):189- 196. Hypoxia, centralization of blood in pulmonary vessels, and increased cardiac output during physical exertion are the pathogenetic pathways of acute pulmonary edema observed during exposure to extraordinary environments. This study aimed to evaluate the effects of breath-hold diving at altitude, which exposes simultaneously to several of the stimuli mentioned above. To this aim, 11 healthy male experienced divers (age 18-52y) were evaluated (by Doppler echocardiography, lung echography to evaluate ultrasound lung B-lines (BL), hemoglobin saturation, arterial blood pressure, fractional NO (Nitrous Oxide) exhalation in basal condition (altitude 300m asl), at altitude (2507m asl) and after breath-hold diving at altitude. A significant increase in E/e’ ratio (a Doppler-echocardiographic index of left atrial pressure) was observed at altitude, with no further change after the diving session. The number of BL significantly increased after diving at altitude as compared to basal conditions. Finally, fractional exhaled nitrous oxide was significantly reduced by altitude; no further change was observed after diving. Our results suggest that exposure to hypoxia may increase left ventricular filling pressure and, in turn, pulmonary capillary pressure. Breath-hold diving at altitude may contribute to interstitial edema (as evaluated by BL score), possibly because of physical efforts made during a diving session. The reduction of exhaled nitrous oxide at altitude confirms previous reports of nitrous oxide reduction after repeated exposure to hypoxic stimuli. This finding should be further investigated since reduced nitrous oxide production in hypoxic conditions has been reported in subjects prone to high-altitude pulmonary edema.

Short-term changes in chest CT images among individuals at low altitude after entering high-altitude environments.

To investigate the short-term changes in chest CT images of low-altitude populations after entering a high-altitude environment. Chest CT images of 3,587 people from low-altitude areas were obtained within one month of entering a high-altitude environment. Abnormal CT features and clinical symptoms were analyzed. Besides acute high-altitude pulmonary edema, the incidence of soft tissue space pneumatosis was significantly higher than that in low-altitude areas. Pneumatosis was observed in the mediastinum, cervical muscle space, abdominal cavity, and spinal cord epidural space, especially the mediastinum. In addition to acute high-altitude pulmonary edema, spontaneous mediastinal emphysema often occurs when individuals in low-altitude areas adapt to the high-altitude environment of cold, low-pressure, and hypoxia. When the gas escapes to the abdominal cavity, it is easy to be misdiagnosed as gastrointestinal perforation. It is also not uncommon for gas accumulation to escape into the epidural space of the spinal cord. The phenomenon of gas diffusion into distant tissue space and the mechanism of gas escape needs to be further studied.

Preliminary study of identified novel susceptibility loci for HAPE risk in a Chinese male Han population.

High altitude pulmonary edema (HAPE) is a life-threatening form of non-cardiogenic pulmonary edema. In recent years, association studies have become the main method for identifying HAPE genetic loci. A genome-wide association study (GWAS) of HAPE risk-associated loci was performed in Chinese male Han individuals (164 HAPE cases and 189 healthy controls) by the Precision Medicine Diversity Array Chip with 2,771,835 loci (Applied Biosystems Axiom™). Eight overlapping candidate loci in CCNG2, RP11-445O3.2, NUPL1 and WWOX were finally selected. In silico functional analyses displayed the PPI network, functional enrichment and signal pathways related to CCNG2, NUPL1, WWOX and NRXN1. This study provides data supplements for HAPE susceptibility gene loci and new insights into HAPE susceptibility.

Altitude illnesses.

Millions of people visit high-altitude regions annually and more than 80 million live permanently above 2,500 m. Acute high-altitude exposure can trigger high-altitude illnesses (HAIs), including acute mountain sickness (AMS), high-altitude cerebral oedema (HACE) and high-altitude pulmonary oedema (HAPE). Chronic mountain sickness (CMS) can affect high-altitude resident populations worldwide. The prevalence of acute HAIs varies according to acclimatization status, rate of ascent and individual susceptibility. AMS, characterized by headache, nausea, dizziness and fatigue, is usually benign and self-limiting, and has been linked to hypoxia-induced cerebral blood volume increases, inflammation and related trigeminovascular system activation. Disruption of the blood-brain barrier leads to HACE, characterized by altered mental status and ataxia, and increased pulmonary capillary pressure, and related stress failure induces HAPE, characterized by dyspnoea, cough and exercise intolerance. Both conditions are progressive and life-threatening, requiring immediate medical intervention. Treatment includes supplemental oxygen and descent with appropriate pharmacological therapy. Preventive measures include slow ascent, pre-acclimatization and, in some instances, medications. CMS is characterized by excessive erythrocytosis and related clinical symptoms. In severe CMS, temporary or permanent relocation to low altitude is recommended. Future research should focus on more objective diagnostic tools to enable prompt treatment, improved identification of individual susceptibilities and effective acclimatization and prevention options.

Pediatric high-altitude pulmonary edema and acute mountain sickness: Clinical features and risk determinants.

This investigation aimed to delineate the clinical manifestations associated with high-altitude pulmonary edema (HAPE) and acute mountain sickness (AMS) in pediatric populations and find the risk factors of HAPE. We conducted a retrospective analysis of clinical data from children under 18 years diagnosed with HAPE and AMS at an average altitude of 3000 m. The clinical data between these two groups were compared. The study encompassed 74 pediatric patients, 27 with AMS and 47 with HAPE. HAPE presentations included classic HAPE (55.3%), reentry HAPE (27.7%), and high-altitude resident pulmonary edema (HARPE, 17.0%). Notably, 87.2% of HAPE cases were male, and 68.1% had a high body mass index (BMI). HARPE instances followed viral infections, prominently SARS-CoV-2. HAPE cases exhibited higher BMI, respiratory tract infections within 1 week preceding symptom onset, an increase in white blood cell counts (WBCs), lower peripheral arterial oxygen saturation (SpO2), and higher heart rate compared to the AMS group. Multivariate logistic regression pinpointed high BMI as an independent HAPE risk factor (odds ratio = 19.389, 95% confidence interval: 1.069-351.759, p = .045). HAPE occurs predominantly in males, with high BMI identified as a critical independent risk factor. The study underscores the need for heightened awareness and preventive strategies against HAPE in children at high altitudes.

Arthroplasty at Very High Altitude with Restricted Resources: Our Experience and Review of Literature.

Patients living in high altitudes are often deprived of total knee arthroplasty (TKA) due to logistic reasons, economic, and social challenges in performing surgical procedures for management of knee pain. Surgical procedures in high-altitude dwellers have associated risk of deep venous thrombosis/pulmonary embolism (DVT/PE). In patients undergoing these procedures at lower altitudes, return to high altitudes can cause high-altitude pulmonary edema (HAPE). We share our experience of performing TKA in high-altitude dwellers by setting up a surgical camp at 11,000 feet. A retrospective assessment of patients undergoing total knee arthroplasty at a camp set up at 11,000 feet between 2014 and 2020 was undertaken. Follow-up data of patients which included clinical assessment by the Knee Society Score (KSS) and complications like DVT, infection, residual deformity, etc. were included in the study. Radiographic evaluation to look for evidence of implant loosening was also inculcated. 132 patients (202 knee joints in 50 male and 82 female patients) underwent TKA during annual camps. The average follow-up of patients was 60months. Mean pre-operative KSS was 38, which was increased to 83 at 1-year follow-up post-surgery. There was no evidence of DVT or superficial or deep infection in any patient in the post-operative period. With this study, we want to highlight that total knee arthroplasty can be safely performed at high altitudes and remote areas with limited health facilities. We believe it is a safer and more convenient prospect for the residents of high-altitude regions. III.

Superoxide dismutase 1-modified dental pulp stem cells alleviate high-altitude pulmonary edema by inhibiting oxidative stress through the Nrf2/HO-1 pathway.

High-altitude pulmonary edema (HAPE) is a deadly form of altitude sickness, and there is no effective treatment for HAPE. Dental pulp stem cells (DPSCs) are a type of mesenchymal stem cell isolated from dental pulp tissues and possess various functions, such as anti-inflammatory and anti-oxidative stress. DPSCs have been used to treat a variety of diseases, but there are no studies on treating HAPE. In this study, Sprague-Dawley rats were exposed to acute low-pressure hypoxia to establish theHAPE model, and SOD1-modified DPSCs (DPSCsHiSOD1) were administered through thetail vein. Pulmonary arterial pressure, lung water content (LWC), total lung protein content of bronchoalveolar lavage fluid (BALF) and lung homogenates, oxidative stress, and inflammatory indicators were detected to evaluate the effects of DPSCsHiSOD1 on HAPE. Rat type II alveolar epithelial cells (RLE-6TN) were used to investigate the effects and mechanism of DPSCsHiSOD1 on hypoxia injury. We found that DPSCs could treat HAPE, and the effect was better than that of dexamethasone treatment. SOD1 modification could enhance the function of DPSCs in improving the structure of lung tissue, decreasing pulmonary arterial pressure and LWC, and reducing the total lung protein content of BALF and lung homogenates, through anti-oxidative stress and anti-inflammatory effects. Furthermore, we found that DPSCsHiSOD1 could protect RLE-6TN from hypoxic injury by reducing the accumulation of reactive oxygen species (ROS) and activating the Nrf2/HO-1 pathway. Our findings confirm that SOD1 modification could enhance the anti-oxidative stress ability of DPSCs through the Nrf2/HO-1 signalling pathway. DPSCs, especially DPSCsHiSOD1, could be a potential treatment for HAPE. Schematic diagram of the antioxidant stress mechanism of DPSCs in the treatment of high-altitude pulmonary edema. DPSCs can alleviate oxidative stress by releasing superoxide dismutase 1, thereby reducing ROS production and activating the Nrf2/HO-1 signalling pathway to ameliorate lung cell injury in HAPE.

Potential therapeutic effects of traditional Chinese medicine in acute mountain sickness: pathogenesis, mechanisms and future directions.

Acute mountain sickness (AMS) is a pathology with different symptoms in which the organism is not adapted to the environment that occurs under the special environment of high altitude. Its main mechanism is the organism's tissue damage caused by acute hypobaric hypoxia. Traditional Chinese medicine (TCM) theory focuses on the holistic concept. TCM has made remarkable achievements in the treatment of many mountain sicknesses. This review outlines the pathogenesis of AMS in modern and traditional medicine, the progress of animal models of AMS, and summarizes the therapeutic effects of TCM on AMS. Using the keywords "traditional Chinese medicine," "herbal medicine," "acute mountain sickness," "high-altitude pulmonary edema," "high-altitude cerebral edema," "acute hypobaric hypoxia," and "high-altitude," all relevant TCM literature published up to November 2023 were collected from Scopus, Web of Science, PubMed, and China National Knowledge Infrastructure databases, and the key information was analyzed. We systematically summarised the effects of acute hypobaric hypoxia on the tissues of the organism, the study of the methodology for the establishment of an animal model of AMS, and retrieved 18 proprietary Chinese medicines for the clinical treatment of AMS. The therapeutic principle of medicines is mainly invigorating qi, activating blood and removing stasis. The components of botanical drugs mainly include salidroside, ginsenoside Rg1, and tetrahydrocurcumin. The mechanism of action of TCM in the treatment of AMS is mainly through the regulation of HIF-1α/NF-κB signaling pathway, inhibition of inflammatory response and oxidative stress, and enhancement of energy metabolism. The main pathogenesis of AMS is unclear. Still, TCM formulas and components have been used to treat AMS through multifaceted interventions, such as compound danshen drip pills, Huangqi Baihe granules, salidroside, and ginsenoside Rg1. These components generally exert anti-AMS pharmacological effects by inhibiting the expression of VEGF, concentration of MDA and pro-inflammatory factors, down-regulating NF-κB/NLRP3 pathway, and promoting SOD and Na + -K + -ATPase activities, which attenuates acute hypobaric hypoxia-induced tissue injury. This review comprehensively analyses the application of TCM in AMS and makes suggestions for more in-depth studies in the future, aiming to provide some ideas and insights for subsequent studies.