High altitude pulmonary edema in children: A systematic review.

INTRODUCTION: High altitude pulmonary edema (HAPE) is a form of acute noncardiogenic pulmonary edema caused by altitude-related hypoxia seen in children as well as in adults. In this systematic review we focus in HAPE occurring in children and adolescents. METHODS: A systematic review was conducted including publications in children 0-18 years of age from three databases up to June 2022. RESULTS: Thirty-five studies representing 210 cases were found. The mean age was 9.8 ± 3.6 years with a male/female ratio of 2.6. The peak age incidence was seen in children between 6 and 10 years old. Only two children (0.9%) were ≤2 years old. The mean altitude in 166 cases was 2861 masl. Only 17 cases (8.1%) occurred at altitudes below 2500 masl. Regarding the different HAPE subtypes there was a predominance of re-entry HAPE (R-HAPE) with 58%, followed by classic HAPE (C-HAPE) with 37.6%. The mean time between arrival and onset of symptoms was 16.5 h. The mortality rate was 1.4%. In 10/28 (36%) of C-HAPE cases there was a structural cardiac/pulmonary anomaly compared to 1/19 (5%) in R-HAPE (p < 0.01). HAPE recurrence was found in 46 cases (21.9%). The involvement in the chest X-rays was seen predominantly in the apices and in the right lung. CONCLUSIONS: R-HAPE was the most common HAPE subtype; HAPE peak age was found between 6 and 10 years of age; HAPE was more frequent in males and was rare in children under 2 years old; associated HAPE structural abnormalities were more common in C-HAPE than in R-HAPE.

Dengue disease in a pediatric patient with severe idiopathic pulmonary hypertension.

Dengue virus can affect the heart, with complications as bradycardia, arrhythmias, and death. We present a case of a 15-year-old patient, diagnosed 4 years before with severe idiopathic pulmonary hypertension, confirmed by catheterism, with continuous follow up. At that time, she was living in Bogotá (2640 m above sea level). Sildenafil and Macitentan were started. She was recommended to live at low altitude and she moved. The patient was transferred back to Bogota, from that place, due to flu-like symptoms and fever. Immunoglobulin M for dengue was confirmed and second-degree atrioventricular block Mobitz I with bradycardia (40 beats/minute) was documented throughout the clinical course. She recovered.

Long-term chronic intermittent hypoxia: a particular form of chronic high-altitude pulmonary hypertension.

In some subjects, high-altitude hypobaric hypoxia leads to high-altitude pulmonary hypertension. The threshold for the diagnosis of high-altitude pulmonary hypertension is a mean pulmonary artery pressure of 30 mmHg, even though for general pulmonary hypertension is ≥25 mmHg. High-altitude pulmonary hypertension has been associated with high hematocrit findings (chronic mountain sickness), and although these are two separate entities, they have a synergistic effect that should be considered. In recent years, a new condition associated with high altitude was described in South America named long-term chronic intermittent hypoxia and has appeared in individuals who commute to work at high altitude but live and rest at sea level. In this review, we discuss the initial epidemiological pattern from the early studies done in Chile, the clinical presentation and possible molecular mechanism and a discussion of the potential management of this condition.

Long-Term Intermittent Work at High Altitude: Right Heart Functional and Morphological Status and Associated Cardiometabolic Factors.

Background: Living at high altitude or with chronic hypoxia implies functional and morphological changes in the right ventricle and pulmonary vasculature with a 10% prevalence of high-altitude pulmonary hypertension (HAPH). The implications of working intermittently (day shifts) at high altitude (hypobaric hypoxia) over the long term are still not well-defined. The aim of this study was to evaluate the right cardiac circuit status along with potentially contributory metabolic variables and distinctive responses after long exposure to the latter condition. Methods: A cross-sectional study of 120 healthy miners working at an altitude of 4,400-4,800 m for over 5 years in 7-day commuting shifts was designed. Echocardiography was performed on day 2 at sea level. Additionally, biomedical and biochemical variables, Lake Louise scores (LLSs), sleep disturbances and physiological variables were measured at altitude and at sea level. Results: The population was 41.8 ± 0.7 years old, with an average of 14 ± 0.5 (range 5-29) years spent at altitude. Most subjects still suffered from mild to moderate symptoms of acute mountain sickness (mild was an LLS of 3-5 points, including cephalea; moderate was LLS of 6-10 points) (38.3%) at the end of day 1 of the shift. Echocardiography showed a 23% mean pulmonary artery pressure (mPAP) >25 mmHg, 9% HAPH (≥30 mmHg), 85% mild increase in right ventricle wall thickness (≥5 mm), 64% mild right ventricle dilation, low pulmonary vascular resistance (PVR) and fairly good ventricle performance. Asymmetric dimethylarginine (ADMA) (OR 8.84 (1.18-66.39); p < 0.05) and insulin (OR: 1.11 (1.02-1.20); p < 0.05) were associated with elevated mPAP and were defined as a cut-off. Interestingly, the correspondence analysis identified association patterns of several other variables (metabolic, labor, and biomedical) with higher mPAP. Conclusions: Working intermittently at high altitude involves a distinctive pattern. The most relevant and novel characteristics are a greater prevalence of elevated mPAP and HAPH than previously reported at chronic intermittent hypobaric hypoxia (CIHH), which is accompanied by subsequent morphological characteristics. These findings are associated with cardiometabolic factors (insulin and ADMA). However, the functional repercussions seem to be minor or negligible. This research contributes to our understanding and surveillance of this unique model of chronic intermittent high-altitude exposure.