Acute High Altitude Pulmonary Edema Research Articles

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.

The Value of CT Examination in the Development of Imaging Manifestations of Acute High Altitude Pulmonary Edema

This study aims to analyze the significance of CT examinations in elucidating the imaging manifestations of acute high-altitude pulmonary edema (HAPE). A cohort of 200 patients with acute HAPE, attending the clinic between January 2021 and January 2022, constituted the subjects. Employing distinct examination methods, participants were categorized into a control group (undergoing X-ray examinations, n = 100) and an observation group (undergoing CT examinations, n = 100). Comprehensive patient data were collected, facilitating a comparative analysis of examination results, diagnosis rates, imaging features, and related indicators between the two groups. No statistically significant differences were evident, signifying comparable profiles (P >0.05). However, the observation group exhibited significantly superior examination outcomes compared to the control group (P < 0.01). The diagnostic rate in the observation group reached 98.00%, surpassing the control group’s nursing efficiency at 92.00%. This observed superiority of the observation group was statistically significant (P < 0.01). While both X-ray and CT methods detected high-altitude pulmonary edema, CT examinations provided clearer insights into specific lesions, enhancing accuracy and diagnosis rates. This study underscores the paramount significance of high-altitude pulmonary edema examinations, particularly advocating for the widespread adoption of CT technology.

Acute high-altitude pulmonary edema in Huaraz: an analytical cross-sectional study

Objective: To describe some epidemiological and clinical characteristics of acute high-altitude pulmonary edema (HAPE) observed in a hospital of the highlands of Ancash, located at 3,052 m a.s.l. Materials and methods: A descriptive observational study conducted with 57 patients who attended the emergency service of Hospital Víctor Ramos Guardia – Huaraz between January 1997 and January 2020. All patients fulfilled Lake Louise Criteria and had a chest X-ray. Median and range were used to analyze the information.Results: Male sex accounted for 91.20 %, ascent HAPE 38.61 % and re-ascent HAPE 61.40 %. Out of all patients, 21.10 % had a history of HAPE, 19.33 % developed a previous respiratory infection, 10.53 % had a concomitant disease, 40.42 % had HAPE during the first quarter of the year and 45 % had been 10 days or less at low altitude. Patients’ clinical presentation included dyspnea at rest, pulmonary crackles, tachypnea, tachycardia and abnormal X-ray in 100 %; productive cough in 96.52 %; chest pain in 92.95 %; headache in 56.11 %; cyanosis in 68.41 %; pink sputum in 42.13 %; fever in 21.13 % and leukocytosis in 60.82 %. The median age was 20 years, respiratory rate 36/min, heart rate 124/min, SBP 100 mmHg, DBP 60 mmHg, temperature 37.2 °C, HGB 17.3 g/dl, HCT 53 %, WBC 12,500/mm3, radiographic resolution of the edema in 48 hours. There were no deaths. Conclusions: The factors that influence HAPE and its determinants are altitude, rate of ascent, genetic factors and history of HAPE.

Acute re-entry high-altitude pulmonary edema

Acute high-altitude pulmonary edema is a potentially life-threatening medical condition. Also known as acute re-entry high-altitude pulmonary edema, it may occur in highland dwellers who return to their hometown after having stayed at a lower-level area. This is the case of a 14 year-old male patient, native to and resident of the city of El Alto (La Paz, Bolivia), located at 4,090 meters above sea level. The patient developed acute high-altitude pulmonary edema when returning from a town at 500 meters above sea level. He required intensive care and showed a favorable evolutio

Letter to the Editor Reply to commentary by G. Sikri and S. Dua on the article "Correlation between single nucleotide polymorphisms in hypoxia-related genes and susceptibility to acute high-altitude pulmonary edema" published in Genetics and Molecular Research 14 (3): 11562-11572 to the letter published in Genet. Mol. Res. 14 (4): 15904-15905.

The object in this study was a Han Chinese population in Lhasa, with 3658 m in altitude from Chengdu, which has 505 m in altitude by air. Within 24 to 48 h before the subjects arrived in the plateau, they completed a basic situation questionnaire, under the guidance of medical staff. Within 24 to 48 h after they reached the plateau, the subjects completed an acute plateau disease questionnaire. The diagnostic standard of HAPE and the diagnosis of acute plateau disease were adopted by the Lake Louise diagnostic standards in 1991 and the Chinese Medical Association promulgated the domestic diagnostic criteria on the Third National Plateau Medical Academic Seminar. Other diseases that cause acute symptoms of altitude sickness, such as plateau pulmonary edema, plateau cerebral edema, acute respiratory infections and neurosis, were excluded. According to the Lake Louise standard, questionnaire and symptom score values >3 points were diagnosed as HAPE. According to the national standard, the questionnaire and symptom score values >5 points were diagnosed as HAPE. At the present, morbidity of HAPE remains relatively high in China. The research shows that usually in the case of not taking preventive measures, according to the factors such as altitude, speed, and time of arrival, the incidence of HAPE is 30% to 90%. Epidemiological survey shows that HAPE happens at an altitude of 2500 m above the plateau. And an altitude of 3000 m above the plateau of China is occupied 1/6 of the total land area, the population of permanent residents is more than sixty million. We detected the 200 cases who adapted to plateau and the 106 cases of patients with HAPE susceptibility genes SNP locus, and got the key SNP loci of HAPE susceptibility genes. We maked the corresponding gene chip diagnostic kits.

Correlation between single nucleotide polymorphisms in hypoxia-related genes and susceptibility to acute high-altitude pulmonary edema.

This study aimed to explore the relationship between genetic changes and high-altitude pulmonary edema (HAPE) susceptibility, and to screen for the key single nucleotide polymorphism (SNP) loci in the HAPE-susceptibility gene, by investigating the SNPs occurring in hypoxia-related genes in HAPE-susceptible and control (non-susceptible) populations. This research was conducted on Han recruits, who travelled to the Lhasa plateau (altitude, 3658 m). Ten loci located on ten genes extracted from the HAPE and healthy populations were amplified by polymerase chain reaction, and subsequently sequenced. The investigated genes included those coding for aldosterone synthase 2 (CYP11B2), angiotensin-converting enzyme (ACE), heat-shock protein 70 (HSP70), nuclear factor kappa B (NF-κB), surfactant protein A2 (SP-A2), plasminogen activator inhibitor-1 (PAI-1), nitric oxide synthetase (NOS), vascular endothelial growth factor (VEGF), prolyl hydroxylase (EGLN1), and zinc finger protein A20. The gene distribution of each SNP loci and its correlation with HAPE was analyzed. Statistical analyses of the genotype frequencies of the SNPs revealed significant differences in the ACE (rs4309), EGLN1 (rs480902), SP-A2 (rs1965708), HSP70 (rs1008438), PAI-1 (rs1799889), and NOS (rs199983) expressions between the HAPE and healthy control groups (P < 0.05); therefore, these SNP loci were believed to indicate HAPE susceptibility. HAPE is correlated with multiple- SNP loci. A correlation analysis between genetic polymorphism and HAPE susceptibility revealed that 6 hypoxia-related genes were key sites accounting for HAPE. These findings could help assess the risk of HAPE in populations expressing different genotypes, in order to reduce the occurrence of HAPE.

Letter to the Editor High altitude pulmonary edema and hypoxia-related genes - Genet. Mol. Res. 14 (3): 11562-11572 “Correlation between single nucleotide polymorphisms in hypoxia-related genes and susceptibility to acute high-altitude pulmonary edema”

Letter to the Editor High altitude pulmonary edema and hypoxia-related genes - Genet. Mol. Res. 14 (3): 11562-11572 “Correlation between single nucleotide polymorphisms in hypoxia-related genes and susceptibility to acute high-altitude pulmonary edema”

Effects of early mechanical ventilation on oxygenation and hemodynamics in acute high altitude pulmonary edema patients complicated by acute respiratory distress syndrome

To investigate the effect of early mechanical ventilation on oxygenation and hemodynamic of acute high altitude pulmonary edema (HAPE) patients complicated by acute respiratory distress syndrome (ARDS). From May 2001 to December 2006, 8 HAPE patients with secondary ARDS admitted to Germud City People's Hospital were enrolled in the study. All the patients received early invasive mechanical ventilation within 24 hours of HAPE. Hemodynamics, cardiac output, arterial and mixed venous blood gas and oxygen dynamics parameters were determined before and after 96 hours of mechanical ventilation. Before treatment the right atrial pressure (RAP), mean pulmonary artery pressure (mPAP), pulmonary vascular resistance index (PVRI) and shunt (Qs/Qt) were above normal values. Oxygen delivery (DO2), oxygen extraction rate (O2ER), and oxygenation index (PaO2/FiO2) were lower than normal values. After treatment with mechanical ventilation, arterial partial pressure of oxygen (PaO2), PaO2/FiO2, arterial oxygen saturation (SaO2), partial pressure of oxygen of mixed venous blood (PVO2) and mixed venous oxygen saturation (SVO2) were increased significantly compared with those before treatment [PaO2: 70.3±2.9 mm Hg (1 mm Hg=0.133 kPa) vs. 49.9±3.5 mm Hg, t=15.292, P=0.001; PaO2/FiO2: 201.6 ± 4.8 mm Hg vs. 134.5±5.2 mm Hg, t=19.618, P=0.004; SaO2: 0.929±0.021 vs. 0.780±0.073, t=6.226, P=0.002; PVO2: 54.8±2.9 mm Hg vs. 44.9±2.6 mm Hg, t=6.767, P=0.002; SVO2: 0.726±0.017 vs. 0.663±0.053, t=3.262, P=0.008]. Heart rate (HR), RAP, mPAP, pulmonary wedge pressure (PAWP), PVRI, right ventricular stroke work index (RVSWI) and Qs/Qt were decreased significantly compared with those before mechanical ventilation [HR: 73±2 bpm vs. 102±13 bpm, t=6.228, P=0.000; RAP: 6.9±1.0 mm Hg vs. 13.9±1.5 mm Hg, t=3.609, P=0.008; mPAP: 18.5±2.9 mm Hg vs. 41.6±3.0 mm Hg, t=4.773, P=0.000; PAWP: 6.9±2.2 mm Hg vs. 14.0±4.2 mm Hg, t=2.747, P=0.030; PVRI: 26.3±1.7 kPa×s×L(-1) vs. 49.6±10.0 kPa×s×L(-1), t=9.861, P=0.000; RVSWI: 11.0±1.9 g×cm(-1)×min×m(2) vs. 22.0±1.5 g×cm(-1)×min×m(2), t=12.704, P=0.000; Qs/Qt: (26±18)% vs. (35±15)%, t=7.603, P=0.000], and cardiac index (CI), DO2, oxygen consumption (VO2) and O2ER were also increased [CI: 71.68±6.67 mL×s(-1)×m(-2) vs. 70.01±6.67 mL×s(-1)×m(-2), t=2.832, P=0.036; DO2 (L×min(-1)×m(-2)): 460.9±14.0 vs. 410.0±3.1, t=9.268, P=0.000; VO2 (L×min(-1)×m(-2)): 158.5±9.2 vs. 129.9±5.3, t=2.818, P=0.004; O2ER: (20±1)% vs. (18±1)%, t=7.652, P=0.000]. All of the 8 patients survived. Pulmonary circulation hemodynamic and oxygen dynamic disorders were found in HAPE patients with secondary ARDS. Treatment with early mechanical ventilation not only improved oxygenation but also reduced pulmonary hypertension and increased cardiac output and DO2.

Elevated plasma atrial natriuretic factor and vasopressin in high-altitude pulmonary edema.

A diagnosis of acute high-altitude pulmonary edema was made in five male skiers (age, 35.0 +/- 1.8 years) by history and physical examination and was confirmed by a characteristic chest radiogram showing alveolar infiltrates associated with a normal cardiac silhouette. Five healthy age- and sex-matched subjects with similar physical activity at the same altitude served as controls. Plasma sodium was 135.0 +/- 1.5 mmol/L in the acutely ill patients compared with 144.0 +/- 3.3 mmol/L in the controls (P less than 0.025). Mean plasma atrial natriuretic factor immunoreactivity averaged 17.6 +/- 5.6 pmol/L in patients with high-altitude pulmonary edema compared with 6.8 +/- 0.7 pmol/L in the controls at the same altitude (P less than 0.05). Elevated atrial natriuretic factor levels normalized to 7.5 +/- 1.9 pmol/L (P less than 0.05) during recovery in Denver (altitude, 1600 meters) 24 hours later. Plasma arginine vasopressin levels were 1.8 +/- 0.37 pmol/L in patients with high-altitude pulmonary edema at diagnosis compared with 0.92 +/- 0.28 pmol/L in controls (P = 0.07). The inappropriately elevated arginine vasopressin levels decreased to 1.29 +/- 0.37 pmol/L during recovery (P less than 0.025), but the lowered plasma sodium concentration had not normalized by discharge within 24-hours of transfer to Denver and averaged 135.8 +/- 1.2 mmol/L. The pathophysiologic implications of these findings are discussed.

Experimental acute high altitude pulmonary edema and the mechanisms of its development

Experimental acute high altitude pulmonary edema and the mechanisms of its development

MOUNTAIN SICKNESS: A CEREBRAL FORM.

Case Studies1 May 1964Mountain SicknessA Cerebral FormRAY F. FITCHRAY F. FITCHSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-60-5-871 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptMountain sickness is a term applied to the various forms of symptomatic physiologic adaptation and maladaptation to medium altitudes. Synonyms include Monge's disease, soroche, and altitude sickness. Hypoxia appears to be the fundamental factor responsible for the development of a spectrum of physiologic responses (1, 2). Forms of this disorder have been classified as acute, subacute, and chronic (3, 4). One of the acute forms, acute high altitude pulmonary edema, has been rather extensively studied in recent years (5-7). Chronic mountain sickness in man and brisket disease in cattle are recognized entities of a more chronic variety (8-10).The following...