高海拔疾病：兒科的特殊考量
統一名詞翻譯
AMS 急性高山病
HAI 高海拔疾病
HACE 高海拔腦水腫
HAPE 高海拔肺水腫
高海拔生理學
在高海拔地區，吸入氧分壓 (PIO2) 降低是氣壓降低的直接結果。隨著 PIO2 的降低，肺泡氧分壓 (PAO2)、動脈血氧分壓 (PaO2) 和動脈血氧飽和度 (SpO2) 也隨之降低，導致組織缺氧。這種缺氧形式被稱為低壓性缺氧，是高海拔疾病 (HAI) 的初始原因。
某些人在反覆攀登同一海拔高度後會發生高海拔肺水腫（HAPE），因此可能存在一個海拔閾值，超過該閾值他們就容易發生HAPE。過去多次發生HAPE的個體表示有遺傳或生理易感性，因此以相同速度攀登至相同海拔高度時，他們有復發的風險。對於這些個體，可以透過降低攀登速度或進行藥物預防來避免復發。
兒童常見的危險因子包括以下幾點：
●急性疾病，伴隨上呼吸道或下呼吸道感染或其他感染（例如，中耳炎）[ 3-7 ]
●先天性心肺疾病[ 8,9 ]（例如，單側肺動脈缺如）[ 10,11 ]；肺動脈高壓[ 3 ]；心臟分流（心房中隔缺損、心室中隔缺損、卵圓孔未閉）
●唐氏症，尤其是伴隨阻塞性睡眠呼吸中止症[ 3,12 ]
●損害呼吸功能的全身性疾病（例如，支氣管肺發育不良[ 13 ]、囊性纖維化[ 14 ]、鐮狀細胞貧血[ 15 ]、嚴重脊椎側彎[ 16 ]、神經肌肉疾病、阻塞性睡眠呼吸中止症）
●足月嬰兒，出生不足六週（早產兒，出生後46週）[ 13,17 ]
●早產兒和足月兒在出生後立即出現呼吸窘迫；一歲以下有吸氧史、支氣管肺發育不良或肺動脈高壓的嬰兒[ 13,17 ]
●HAPE 患者容易再次發生高山症（HAPE 患者居住在高海拔地區 [2500 米，8200 英尺以上]，在低海拔地區短期旅行 [例如，幾天到幾週]，然後迅速從低海拔地區返回家中）[ 18,19 ] 。
伴隨肺動脈血流量增加的心臟病變－患有伴隨肺動脈血流量增加或肺動脈高壓的心臟病變的嬰幼兒發生高海拔肺水腫的風險增加。右肺動脈孤立性缺如與在相對低海拔地區發生高海拔肺水腫有關，這些患者應避免暴露於高海拔地區[ 10,29 ]。其他可增加肺血流量的心臟缺陷，例如房間隔缺損、室間隔缺損和動脈導管未閉，也可能增加發生高海拔肺水腫的風險，並可能受益於氧飽和度監測[ 25,30 ]。
另一方面，雖然有報告指出卵圓孔未閉 (PFO) 與 HAPE 之間存在關聯，但因果關係尚未確定，PFO 也不被認為是高海拔暴露的禁忌症
唐氏症－21三體症兒童除了先天性心臟缺陷風險增加外，肺血管反應性增強，肺動脈高壓風險也較高。他們也更容易出現阻塞性睡眠呼吸中止症和通氣不足。這些因素可能導致即使在相對較低的海拔，他們發生高海拔肺水腫（HAPE）的風險也更高[ 3 ]。因此，對於21三體症患兒，應謹慎安排高海拔旅行[ 25 ]。
●有氧療史或肺動脈高壓史的嬰兒－1歲以下有氧療史或肺動脈高壓史的嬰兒存在一些獨特的生理限制，使他們在快速暴露於高海拔（3000至5000米[9840至16400英尺]）時，容易發生低氧血症、嚴重肺動脈高壓，在極端情況下會發生右心衰竭
兒童AMS
AMS是最常見的高山症。 AMS的風險取決於個體的易感性、到達的海拔高度以及上升速度。因此，雖然在海拔2000米（6560英尺）以下AMS並不常見，但在海拔2000米至3000米（6560至9840英尺）的睡眠海拔範圍內，AMS卻相當常見（成人和兒童的發病率約為25%），而美國西部的一些城市和大多數滑雪勝地就位於這一海拔高度（表 3-32） [323-36] 3-366 ] 3-3623-36213-323-32713-3276 7607年）。在大多數情況下，可以透過適當的預防措施來預防兒童HAI，或在出現嚴重疾病（例如HAPE或HACE前進行治療。
在高海拔地區，一些小型觀察性研究最初表明，兒童和青少年在數小時內從海平面上升到海拔3500公尺以上時，發生急性高山症的頻率可能高於成人[ 33,37,38 ]。然而，更大規模的研究發現，兒童和青少年發生急性高山症的頻率與成人相同或更低：
●一項觀察性研究評估了快速攀登對家庭的影響，該研究納入了157名兒童，他們在2.5小時內攀登了3450公尺。結果顯示，兒童發生急性高山症（AMS）的比例（30%）低於青少年（37%）和成人（45%）[ 39 ]。此外，家族聚集性表現穩定，可解釋25%至50%的變異性，這是AMS遺傳影響的首個證據。
●在另一項針對 48 名接受相同快速上升方案的兒童的研究中，6 小時時急性高山症發生率為 25%，18 小時時為 21%，42 小時時為 8%；所有急性高山症均為輕度，且均無需下降 [ 40 ]。
●第三項研究讓 118 名 6 至 16 歲的兒童在 2.5 小時內到達阿爾卑斯山 3450 公尺的高度，結果發現 40 小時內僅有 6% 的兒童出現急性高山症，證實了急性高山症無需治療即可迅速緩解 [ 41 ]。
因此，兒童急性高山症的整體風險似乎與成人相同或更低，而且與成人一樣，較慢的上升速度可以降低罹病風險。
成人急性高山症的流行病學將在另一章節中進行更詳細的討論。 （請參閱 「急性高山症與高海拔腦水腫」章節中的「流行病學與危險因子」部分。）
急性高山症 （ AMS）和高海拔腦水腫（HACE）通常被認為是同一疾病譜上的兩個階段，具有相同的潛在病理生理機制。儘管這種病理生理機制的某些方面仍不清楚，但AMS/HACE代表一個連續光譜，並且AMS可發展為致命的HACE這一概念符合臨床經驗，有助於疾病管理。然而，尤其是在幼兒和嬰兒中，由於難以識別非語言兒童的症狀（例如頭痛），AMS的識別受到阻礙。某些兒科患者（例如，6週齡以下的嬰兒、患有先天性心臟病、囊性纖維化或唐氏症的兒童）也更容易患上危及生命的疾病。 （請參閱上文「針對患有既往疾病的兒童的建議」。）
臨床表現 － 幼兒急性代謝症候群的症狀不具特異性，包括玩耍減少、臉色蒼白、煩躁不安、睡眠品質差、嘔吐和食慾下降[ 27,34,35 ]。
在年齡較大的兒童和青少年中，高山症的症狀與成人相似；最常見的症狀是頭痛，可能伴隨或隨後出現呼吸困難、頭暈、睡眠品質差、厭食、疲勞、噁心和嘔吐[ 36 ]。成人急性高山症的臨床表現和診斷將在其他章節中詳細討論。 （請參閱 「急性高山症與高海拔腦水腫」章節中的「臨床特徵」部分。）
急性高山症通常在到達高海拔地區後6至12小時出現，但也可能在1至2小時內或24小時後出現[ 42,43 ]。如果沒有進一步上升，症狀通常在第一個晚上最為嚴重，休息一天後（例如，停止滑雪或遠足）一般會緩解，並且不會在同一海拔高度復發。但上升到更高海拔時，急性高山症可能會再次出現。有時，即使沒有進一步上升，急性高山症的症狀也可能持續數天。在這種情況下，如果標準治療無效，則需要下降。 （請參閱 「急性高山症與高海拔腦水腫」章節中的「急性高山症」部分。）
補充氧氣可用於輔助急性高山症的臨床診斷。根據我們的經驗，在採取其他幹預措施之前，透過鼻導管以 2 至 4 公升/分鐘的流量給予氧氣 15 至 20 分鐘，可顯著改善頭痛和其他症狀；短暫下到較低海拔地區也有類似效果，尤其對年幼兒童而言。
如果症狀在到達特定海拔高度兩天後才出現，且無頭痛、靜止時呼吸困難，以及吸氧後症狀未迅速改善，則臨床醫生應考慮其他診斷。除非急性高山症的診斷不明確，否則通常無需進行影像學或實驗室檢查。其他需要考慮的原因包括一氧化碳中毒、偏頭痛（包括新發偏頭痛）、脫水、疲勞、低鈉血症、病毒感染、細菌感染（如肺炎或中耳炎）以及隱性外傷，例如角膜擦傷。在幼兒中，急性高山症的診斷是一種排除性診斷。
單純的急性高山症不會導致體溫升高，因此，對於在高地地區出現發燒症狀的兒童，應根據其年齡和免疫接種情況進行適當的發燒評估。臨床醫師應密切觀察兒童的徵兆和對氧氣的反應，如有疑問，應傾向於延長觀察期，然後再將症狀歸因於急性高山症以外的其他疾病。 （請參閱 “3至36個月大兒童不明原因發燒：評估和處理”，其中“外觀良好的患者”部分。）
診斷 － 急性高山症的診斷主要依據典型的臨床表現，包括嘔吐、疲倦、蒼白、頭痛、煩躁不安和/或呼吸困難，這些症狀通常在抵達高海拔地區後24小時內出現，且排除其他病因（例如中耳炎、肺炎或病毒感染）。吸氧或下降海拔後症狀迅速改善可支持診斷。
治療 － 兒童高山症的治療原則與成人相同[ 44 ]。所有高山反應都會隨著下降而緩解，儘管並非總是必須下降。我們發現，下降500公尺（1600英尺）對大多數兒童來說就足夠了。重要的是，團隊成員和患者本人要時刻警惕任何症狀或病情惡化的跡象，尤其是在海拔4000公尺（13120英尺）以上，因為急性高山症可能迅速發展為高山腦水腫（HACE）。
院內獲得性感染的治療取決於症狀的嚴重程度：
●輕度高山症－輕度高山症可採用保守治療，包括症狀治療（例如，服用乙醯胺酚或布洛芬緩解頭痛，服用昂丹司瓊緩解嘔吐，以及休息和補充水分）。通常無需下降。
●中重度急性高山症－中重度急性高山症（即休息或對症治療無效，或症狀為中重度）可能需要下山或吸氧（如有條件），和/或使用特定藥物（表3）。吸氧至少2至4小時效果最佳，但我們通常建議吸氧12至24小時，氧流量應足以維持血氧飽和度（SpO2）在90%至92%之間（通常為1至2公升/分鐘）。如果無法吸氧，且下山延遲或不切實際，則應給予地塞米松，通常持續24小時（表3）。兒童患者若症狀持續或經治療後加重，則必須下山。
●高山肺水腫 (HAPE) – 與成人一樣，兒童高山肺水腫的治療需要下降海拔和/或吸氧。
●HACE－在極少數疑似兒童HACE的情況下，應立即下撤。補充氧氣、地塞米松和高壓氧治療可以暫時緩解病情，直到完成撤離（表3）。
預防和藥物預防 － 適應環境和緩慢上升是避免高山症的最佳方法。建議前往高海拔地區滑雪、健行或攀岩的旅客在抵達後的頭幾天限制活動。充足的水分攝取也很重要，但應避免過度補水以預防低鈉血症。
為預防急性高山症（及其他高海拔相關症候群），專家建議切勿在一天之內從低海拔地區前往（或在）海拔2750公尺（9000英尺）或更高的地方。此外，已在海拔2500公尺（8200英尺）以上的人，其睡眠海拔不應比前一晚的海拔高出500公尺（1640英尺）以上。對於曾在以往登山過程中出現急性高山症或其他高山症相關問題的人來說，這種方法尤其重要；這些人再次接觸高海拔地區時更容易出現這些疾病。
乙醯唑胺預防 － 尚未有研究探討乙醯唑胺預防性藥物治療在快速上升至海拔3450公尺的兒童的應用。一項前瞻性觀察研究納入了48名快速上升至海拔3450公尺的較大兒童和青少年，結果發現其中18名（38%）出現急性高山症（AMS）症狀，但無一例患者需要接受特殊藥物治療或撤離至較低海拔 [ 40 ]。研究提示，對於大多數未適應高海拔環境的健康較大兒童和青少年，預防性治療可能並非必要。
如果使用乙醯唑胺，治療持續時間取決於上昇路線。對於計劃攀登至固定睡眠海拔高度的人員（例如休閒滑雪者），可在攀登前一天開始服用乙醯唑胺，並持續服用48小時。如果計劃繼續攀登，則可繼續服用乙醯唑胺直至達到最高海拔。乙醯唑胺也可在上升過程中的任何階段間歇性服用，以加速適應海拔或治療輕度急性高山症。在同一海拔高度停藥後，症狀不會復發。雖然經過幾天的適應後，急性高山症的風險會降低，但乙醯唑胺仍可能有助於睡眠。
兒童預防急性高山症（AMS）的乙醯唑胺劑量為每次1.25 mg/kg，每日兩次（單次最大劑量125 mg）（表3）[ 44 ]。對磺胺類抗生素過敏的禁忌症已受到質疑，此類患者服用乙醯唑胺發生過敏性休克的風險似乎不高。另一方面，先前對磺胺類抗生素發生史蒂文斯-約翰遜反應的機制與過敏性休克不同，因此一些臨床醫生選擇不對這類患者使用乙醯唑胺。
高海拔腦水腫 （ HACE）是一種罕見的危及生命的高海拔疾病，理論上可能發生在兒童身上[ 45 ]。在成人中，HACE通常發生在海拔3000至3500公尺（9840至11480英尺）以上的急性高山症（AMS）和/或高海拔肺水腫（HAPE）患者中，具體內容將在其他章節中詳細討論。
高海拔肺水腫 （ HAPE）是一種非心因性肺水腫，可能致命。在美國，低地兒童前往落基山脈高海拔度假勝地後發生HAPE的機率尚不清楚。 HAPE的整體發生率約為萬分之一，其中許多是兒童[ 46 ]。 HAPE可分為三種不同的類型：
●經典型高海拔肺水腫 (cHAPE)—這種類型的肺水腫通常發生在從低海拔上升到高海拔的人群中，或發生在高海拔地區快速上升到更高海拔的人群中。 cHAPE 常見於快速上升到海拔 2500 公尺（8200 英尺）以上睡眠海拔的人群 [ 1 ]，但海拔高度本身不應作為排除該診斷的依據 [ 46 ]。
●重返高海拔肺水腫（rHAPE）－這種疾病常見於從低海拔地區返回家鄉的高海拔居民。
●高海拔居民肺水腫（HARPE）－這種疾病是由高海拔居民在無海拔變化的情況下發生急性呼吸道感染而引發的。
如下列研究所示，居住在高海拔地區然後暫時下降的兒童有高海拔肺水腫的風險。患有急性病毒性上呼吸道感染的兒童前往高海拔地區旅行或居住在高海拔地區，患病風險可能略有增加[ 4,5,18,28,47-49 ]：
●一項回顧性研究分析了科羅拉多州利德維爾市（美國海拔最高的永久居住地，海拔3094米，即10152英尺）32名因高海拔肺水腫（HAPE）住院的患者共39次發作的情況。研究發現，32名患者中有25名年齡在15歲以下，除2名患者外，其餘均為利德維爾市的常住居民[ 18 ]。大多數發作發生在短暫下降到較低海拔之後；其中3名患者的下降時間僅為24小時。研究也發現，HAPE的發生率隨年齡增加而降低，這提示兒童肺血管對海拔的某種未知反應可能是導致兒童HAPE高發生的原因之一。
●在一項針對安第斯山脈 97 名受害者的研究中，也描述了類似的兒童 HAPE 盛行率較高；2 至 12 歲的兒童比年齡較大的患者肺水腫更為嚴重 [ 49 ]。
●一項觀察性研究報告了科羅拉多州利德維爾市七名已從高海拔肺水腫（HAPE）中康復的兒童的心導管檢查結果[ 4 ]。其中三名兒童患有與病毒性上呼吸道感染相關的HAPE，先前並無高山症史。這些患者在缺氧時平均肺動脈壓升高。
●在登山前不久發生的上呼吸道感染（感冒、支氣管炎或中耳炎）似乎也會使居住在低海拔地區的兒童更容易患上高海拔肺水腫（HAPE）；這種現象可能與感染期間發炎介質的釋放有關[ 5 ]。此外，兒童的肺血管反應性比成人更高，發炎會增加毛細血管通透性。這些因素共同導致兒童更容易發生肺水腫。
臨床表現 － 在幼兒中，高海拔肺水腫（HAPE）通常表現為呼吸窘迫在1至2天內逐漸加重，但也可能進展得更為迅速。幼兒和嬰兒可能只表現為蒼白、意識模糊或其他非特異性症狀，例如煩躁不安、哭鬧、食慾下降、玩耍減少、睡眠紊亂，甚至嘔吐[ 6,25,34,35 ]。在嬰兒中，肺動脈壓升高和胎兒分流（無論是否合併HAPE）均可導致嚴重的低氧血症。因此，脈搏血氧飽和度可能低於該海拔的正常值。表4列出了不同海拔和不同暴露條件下動脈血氣分析結果和氧飽和度的平均值和正常值範圍，以幫助解讀結果。 （請參閱 「高海拔肺水腫」章節中的「病理生理學」部分。）
在年齡較大的兒童和青少年中，高海拔肺水腫可能表現為隱性咳嗽、疲乏、與工作量不成比例的呼吸困難、靜止時呼吸困難以及咳出泡沫狀、常呈鐵鏽色的痰液。此時的身體檢查結果包括呼吸急促、紫紺、心搏過速以及肺部聽診可聞及瀰漫性囉音。如有條件，胸部X光片可顯示瀰漫性間質性改變，這是心源性肺水腫的典型表現。 （參見 「非心因性肺水腫」。）
高海拔肺水腫可能在數小時或數天內逐漸出現，但也可能突然發作。它最常發生在高海拔停留兩晚之後。高海拔肺水腫也可能在沒有急性高山症的情況下發生。
單純由高海拔肺水腫引起的體溫升高超過 38.3°C 並不常見；體溫升高應考慮是否有併發感染或其他疾病。對於發燒較高的幼兒，應根據其年齡和免疫接種情況進行評估。然而，呼吸道感染和高海拔肺水腫可能同時存在。
兒童的鑑別診斷包括肺炎、心臟衰竭和其他非心臟性肺水腫。
診斷 — 高海拔肺水腫 (HAPE) 的診斷依賴於典型的臨床表現，包括咳嗽、疲乏、呼吸困難、泡沫痰、肺部聽診可聞及瀰漫性囉音、呼吸窘迫和/或特定海拔高度的低氧血症（表 4），這些症狀通常在高海拔暴露後 1 至 2 天內出現肺炎，且無其他病因（例如肺炎）。在嬰幼兒中，HAPE 可能伴隨其他非特異性急性高山症 (AMS) 症狀，例如煩躁不安、活動減少、食慾減退和嘔吐。如果進行胸部 X 光檢查，則可見瀰漫性間質性改變，符合非心因性肺水腫的表現。
實驗室檢查結果可能包括白血球增多（可能由低壓低氧壓力反應引起）和C反應蛋白升高；這些結果可能提示臨床醫師考慮治療合併感染性疾病[ 50-52 ]。此外，B型鈉尿肽和肌鈣蛋白可能會輕度升高，但通常會隨著病情緩解而迅速恢復正常。
治療 － 對於從低地升到高海拔地區的兒童，HAPE 的治療目標與年齡較大的患者相同：透過增加吸入氧分壓來迅速降低肺動脈 (PA) 壓力和低氧血症 [ 44,53 ]。
選項包括：
●限制體力消耗和寒冷暴露
●透過氧氣罐或製氧機提供補充氧氣
●撤離到較低海拔
●利用高壓氧療法模擬下降
●硝苯地平（≥50 kg）或氨氯地平（<50 kg 或 <17 歲）（表 3）
在這些治療方法中，下降（模擬或實際下降）和/或補充氧氣通常單獨使用最為有效，且似乎優於任何藥物治療。在一些度假區，患有高海拔肺水腫的兒童作為門診病人接受補充氧氣治療，並與家人一起留在原海拔高度，接受密切追蹤。硝苯地平或氨氯地平也被推薦使用（表3）[ 25,46,53 ]。與硝苯地平相比，氨氯地平的優點在於每日一次給藥，且有液體或適當大小的片劑形式，因此更適合幼兒使用。 （請參閱 「高海拔肺水腫」部分的「治療」章節。）
對患有 HAPE 的兒童不當地使用抗生素和利尿劑是無效的，應該避免[ 46 ]。
對於病情嚴重的兒童，尤其是意識障礙的患兒，可能需要透過高流量鼻導管或非侵入性通氣進行吸氧。氣管插管的情況很少見。值得注意的是，重症兒童的病情可能需要一到兩個小時才能明顯好轉，氧氣需求量也會減少。
一小部分患有高海拔肺水腫 (HAPE) 的兒童可能存在潛在的易感疾病。一項研究顯示，17% 的 HAPE 兒童在接受超音波心臟檢查後被診斷出新的心臟結構異常（例如卵圓孔未閉 [PFO] 和房間隔缺損 [ASD]）[ 46 ]。因此，建議進行超音波心臟檢查以評估是否有潛在的肺動脈高壓，並排除已知的危險因素，例如房間隔缺損、導管起源的孤立性肺動脈、主動脈縮窄、室間隔缺損和肺靜脈狹窄 [ 30,46 ]。卵圓孔未閉 (PFO) 可能是危險因素，取決於其大小。
預防 － 與急性高山症一樣，緩慢上升是預防高海拔肺水腫的最佳方法。曾患過高海拔肺水腫的人員應被鼓勵緩慢上升，並做好一旦出現高海拔肺水腫症狀就迅速下降的準備。 （請參閱 「高海拔肺水腫」章節中的「預防」部分。）
對於居住在低海拔地區且無高海拔肺水腫（HAPE）病史的健康兒童，我們建議進行充分的適應性訓練，不建議使用藥物預防HAPE。一些專家基於成人資料和藥物類別效應，建議對易感兒童使用硝苯地平或氨氯地平預防HAPE[ 53 ]。然而，鈣通道阻斷劑在兒童預防HAPE的研究尚不充分。硝苯地平是預防易感成人HAPE的首選藥物，但市售硝苯地平製劑的劑量對兒童而言過大[ 26 ]。在極少數情況下，如果兒童曾發生過HAPE且無法緩慢上升，則使用氨氯地平進行預防可能是合理的選擇。劑量為每日一次口服2.5至5毫克（6至17歲且體重≥25公斤的兒童）或每日一次口服0.1至0.6毫克/公斤/次（最大劑量5毫克/天；1至5歲或體重<25公斤的兒童）。理想情況下，預防性用藥應在登山前24小時開始，並在目的地海拔持續5天（表3）。在高風險情況下，治療可能需要更長時間。
科羅拉多州臨床醫生的經驗表明，乙醯唑胺預防復發性高海拔肺水腫（HAPE）兒童可能有效（表3）。雖然尚未進行正式研究，但已知乙醯唑胺可降低上升至高海拔時的肺動脈壓，並加速適應過程。一些專家建議使用較低的預防劑量（1.25 mg/kg 而非 2.5 mg/kg，每日兩次）。然而，該較低劑量是基於成人研究得出的，在獲得更多兒科特異性數據之前，我們不建議使用該劑量。
其他高海拔相關疾病 － 高海拔視網膜出血和高海拔睡眠週期性呼吸是兒童可能發生的其他高海拔疾病類型。此外，由於兒童體表面積與體重的比值較大，且體內肝醣儲備較少，難以滿足寒冷天氣下增加的能量需求，因此他們更容易發生體溫過低。若照顧者未能妥善保暖，避免兒童暴露於寒冷環境中，幼兒也容易發生凍傷。
高海拔肺動脈高壓 － 嚴重的高海拔肺動脈高壓（HAPH）在健康嬰幼兒中較為罕見。然而，出生少於六週的嬰兒尤其容易發生肺動脈高壓，並可能進展為右心衰竭[ 54 ]。據報道，在出生或抵達海拔3000至5000米（9840至16400英尺）並停留超過一個月的低海拔父母所生的嬰兒中，高達1%的人會患上這種疾病；該病幾乎僅發生於這一群體[ 25 ]。有鑑於此疾病的風險，對於通常生活在低海拔地區或主要在低海拔地區妊娠的六週以下嬰兒，應避免其長時間暴露於高海拔地區[ 32 ]。
6週至1歲的嬰兒若長期暴露於高海拔地區，發生肺動脈高壓伴隨低氧血症、動脈導管未閉（PDA）及卵圓孔未閉（PFO）的風險可能較高[ 13,55 ]。對於將長期停留在高海拔地區的嬰兒，應進行身體檢查和初始脈搏血氧飽和度測量，並在兒童保健就診時定期監測。身體檢查結果提示肺動脈高壓（例如，收縮期噴射性雜音伴隨單音或狹窄分裂的第二心音）或其他結構性心臟病的患者應進行心電圖檢查。如果臨床表現提示結構性心臟病或肺動脈高壓，則還需進行超音波心臟檢查。 （請參閱 「兒童肺動脈高壓：分類、評估和診斷」中的「評估」部分。）
高海拔視網膜出血 － 高海拔視網膜出血（HARH）在海拔4270公尺（14005英尺）以上較為常見，但通常無症狀，因此除非黃斑部受累，否則不易被發現。患者通常主訴視力模糊，眼底檢查可見火焰狀視網膜出血。 與其他高海拔疾病一樣，緩慢上升是預防方法，下降是最佳治療方法。目前尚無藥物可以預防或治療高海拔視網膜出血。任何出現影響視力的出血患者都應下降。視網膜出血會在數週至數月內緩慢消退。
高海拔睡眠週期性呼吸 － 高海拔睡眠週期性呼吸是一種陳-施氏呼吸，幾乎只發生在非快速動眼睡眠期，如果過度換氣階段足夠強烈，可能導致受試者覺醒。兒童可能比成人更不容易出現這個問題。例如，一項針對20名9至12歲兒童及其父親的觀察性研究，比較了他們在海拔3450公尺（11316英尺）和490公尺（1607英尺）睡眠期間的呼吸感應容積描記法、脈搏血氧飽和度和呼氣末二氧化碳測量值。研究發現，與成人相比，兒童的週期性呼吸明顯減少，但過度換氣和夜間血氧飽和度下降的情況與成人相似[ 33 ]。此外，在研究過程中，50%的兒童符合急性高山症（AMS）的診斷標準，而成人的比例為30%。這項發現表明，這些兒童表現出的更穩定的呼吸模式與較低的二氧化碳呼吸暫停閾值有關，但這並不意味著他們對高海拔的耐受性更強。 （請參閱 「高海拔疾病：生理、危險因子和一般預防」一節中的「其他與海拔相關的疾病」。）
給家長/監護人的旅遊建議
健康的嬰兒和兒童 － 六週以上的健康嬰兒和幼兒，包括氣喘控制良好的幼兒，通常都能很好地耐受高海拔旅行，很少會患上嚴重的高海拔病（HAI）。
臨床醫師應避免6週齡以下、出生地或懷孕期間主要在低海拔地區（<1500公尺[4920英尺]）的嬰兒前往高海拔地區旅行，因為他們有突發性嚴重低氧血症、肺動脈高壓和右心衰竭的風險。 （請參閱上文「危險因子」及「高海拔腦水腫」。）
以下措施可降低幼兒發生院內感染的風險或便於管理[ 17 ]：
●逐步上升－一般來說，居住在海拔1500公尺（4920英尺）以下的人應避免突然上升到海拔2750公尺（9000英尺）以上的睡眠地點。最好的方法是在海拔1600米至2200米等中間高度停留一晚（尤其是在前往之前曾引起症狀的海拔高度時）。兩晚則更佳。 （請參閱上文「預防和藥物預防」以及 「高山症：生理、危險因子和一般預防」中關於「逐步或分階段上升」的部分。）
●前兩天避免過度勞累－劇烈的健行、滑雪等活動，應在適應高海拔環境一到兩天後再進行。如果必須進行劇烈運動，例如需要背負重物的健行，攀登速度更需放慢。
●乙醯唑胺預防－大多數專家不會常規地為健康兒童或成人開立乙醯唑胺預防性藥物，尤其是在他們逐漸上升到高海拔地區的情況下[ 1 ]。在無法逐漸上升的情況下（例如，搭乘飛機快速上升到海拔2750公尺[9000英尺]以上的目的地），以及既往在類似海拔和上升速度下反覆出現急性高山症（AMS）的兒童，可能需要進行預防性用藥。然而，兒童既往AMS病史並不能可靠地預測再次發病[ 56 ]。 （請參閱上文「乙醯唑胺預防」。）
●症狀治療－家長或其他照顧者應隨身攜帶布洛芬。適量的布洛芬可以迅速緩解幼兒的煩躁不安或減輕大齡兒童的頭痛。
必要時，也可以開立昂丹司瓊，尤其是在患者睡眠海拔超過 9000 英尺或參加長途跋涉時。
●下降途徑的可用性－如果發生嚴重的高海拔感染，應能迅速採取下降措施。對於難以快速下降的目的地，需要謹慎行事並做好計劃。
●醫療資源－度假社區通常擁有具備醫院感染（HAI）專業知識的醫療保健人員，他們能為家長或其他照顧者提供極佳的醫療資源。如果在這些場所確診醫院感染，通常可以進行有效控制，從而使旅程得以繼續。
臨床醫師應建議照顧者評估偏遠地區的緊急救援或醫療照護能力，以判斷其子女發生醫院感染的風險。
透過適當的教育，大多數家長和照顧者都能辨識出醫院獲得性感染的危險因子、症狀和體徵，即使是語言發展前的兒童也能辨識[ 35 ]。這些知識可以幫助照顧者判斷急性高山症（AMS）的可能性，並依照上述方法進行應對[ 17 ]。 （參見上文「急性高山症」。）
照顧者也應了解，如果患者出現精神狀態改變，例如明顯嗜睡、呼吸困難或共濟失調，應立即就醫。
對於出現輕度 AMS 症狀，可透過下降或藥物治療緩解的兒童，不需要進行特殊評估 [ 17 ]。
通常居住在高海拔地區的兒童，如果出現嚴重的低氧血症或高山肺水腫（HAPE），則需要評估是否有肺動脈高壓或結構性心臟異常[ 4,9 ]。
易感嬰幼兒 － 應建議患有以下疾病的兒童的父母或其他照顧者避免前往高海拔地區旅行[ 13,17 ]（見上文「危險因子」）：
●足月但出生少於六週的嬰兒（早產兒指胎齡不足46週的嬰兒）或有氧療史或肺動脈高壓病史的足月但年齡不超過一歲的嬰兒
●胎齡超過46週且有氧療史、支氣管肺發育不良或肺動脈高壓的早產兒
●先天性心臟病伴隨肺動脈高壓、紫紺或心內分流
●鐮形血球貧血症
●唐氏症合併心臟分流或肺動脈高壓
●活動性呼吸系統疾病，如肺炎、微支氣管炎或囊性纖維化急性惡化
病情穩定的囊性纖維化兒童若能在旅行期間進行脈搏血氧飽和度監測並提供吸氧，則可能可以前往高海拔地區旅行。對於六歲以上的兒童，可以進行第一秒用力呼氣容積（FEV1 ）評估和低氧吸入試驗，這有助於識別哪些兒童在旅行期間需要吸氧[ 26 ]。幾乎所有度假區都有家用氧氣公司，可以接受執照醫生開立的氧氣處方。照顧者應確保兒童在旅行期間嚴格遵守既定的胸部物理治療、祛痰和抗生素治療方案。
患有神經肌肉疾病或限制性肺病（例如嚴重的脊椎側彎）的兒童在旅行前應由兒科肺科醫生進行評估，以確定在高海拔地區是否需要支持措施，例如補充氧氣（持續或夜間）或夜間雙水平正壓通氣[ 26 ]。
病人須知
UpToDate 提供兩種類型的病患教育資料：「基礎知識」和「進階知識」。 「基礎知識」系列文章語言淺顯易懂，閱讀難度相當於小學五六年級水平，解答患者可能對特定疾病提出的四五個關鍵問題。這些文章最適合希望了解疾病概況且偏好簡短易讀資料的患者。 「進階知識」系列文章篇幅更長、內容更深入、更詳細。這些文章的閱讀難度相當於小學十年級至十二年級水平，最適合希望獲得更深入資訊且能夠理解一些醫學術語的患者。
以下是一些與此主題相關的病患教育文章。我們鼓勵您列印或透過電子郵件將這些文章發送給您的患者。 （您也可以透過搜尋「病患資訊」和您感興趣的關鍵字，找到各種主題的病患教育文章。）
●基礎知識主題（參見 「病患教育：高山症（基礎）」）
總結與建議
●海拔高度與高山症風險－高山症的風險取決於個體的易感性、上升速度和到達的海拔高度。海拔超過2500公尺（8200英尺）可能與兒童高山症有關。然而，大多數健康兒童在海拔低於3500公尺（11480英尺）的地方通常不會出現任何嚴重症狀。 （參見上文「兒童高山症」。）
●HAI 的危險因子– 特別容易發生嚴重 HAI 的兒童包括以下幾類
•六週齡以下的嬰兒
•一歲以下有吸氧史或肺動脈高壓病史的嬰兒，包括早產兒
•居住在高海拔地區並經歷短暫下降的兒童
•患有唐氏症、先天性心臟病、囊性纖維化或神經肌肉疾病而影響通氣功能的兒童
健康的兒童在攀登至極高海拔地區（超過3500公尺[11480英尺]）時，應緩慢進行，並且只有在出現問題時能夠迅速下降的情況下才應進行。 （請參閱上文「攀登建議」。）
●給家長/監護人的旅行建議－健康兒童通常能很好地適應高山症旅行，很少出現嚴重的高山症。臨床醫師應告知家長或其他監護人，度假社區通常有擅長處理高山症相關問題的醫護人員，如果他們懷疑孩子可能出現高山症，這些醫護人員是很好的資源。 （請參閱上文「給家長/監護人的旅遊建議」。）
INTRODUCTION
This topic will review the unique pediatric aspects of high-altitude illness (HAI).
The different types of HAI, their pathophysiology, and methods for prevention and treatment are discussed separately.
●(See "High-altitude illness: Physiology, risk factors, and general prevention".)
●(See "Acute mountain sickness and high-altitude cerebral edema".)
●(See "High-altitude pulmonary edema".)
●(See "Approach to patients with heart disease who wish to travel by air or to high altitude".)
BACKGROUND
Every year, the beauty and recreational opportunities of the mountains attract millions of visitors from lowland elevations to high-altitude destinations worldwide. Resort towns in the Western United States alone attract over 30 million visitors annually, generally to sleeping elevations of 2000 to 3000 m (6560 to 9840 feet). Many more millions visit cities at these elevations, including several large cities in South America and Asia situated above 3000 m (9840 feet) (table 1) [1]. Most of these destinations can be reached within a day using modern means of transportation. Many of these mountain travelers are children.
Rapid ascents to high altitude place the unacclimatized child at risk for developing high-altitude illness (HAI). Clinicians working in mountainous areas must familiarize themselves with the presentation and management of HAI in children, while all health care workers who advise travelers need to understand the best prevention strategies and treatment options. The clinician advising families with children on wilderness and high-altitude trips should offer an organized pre-trip evaluation that evaluates individual risk factors, provides recommendations for measures to prevent HAI, and determines whether prophylactic medication is appropriate [2]. (See 'Patient risk assessment and mitigation' below and 'Prevention and pharmacologic prophylaxis' below and 'Travel advice for parents/caregivers' below.)
HIGH-ALTITUDE PHYSIOLOGY
Diminished inspired partial pressure of oxygen (PIO2) at altitude is the direct result of lower barometric pressure. As PIO2 decreases, so does the partial pressure of alveolar oxygen (PAO2), arterial PO2 (PaO2), and arterial oxygen saturation (SpO2), resulting in tissue hypoxia. This form of hypoxia is termed hypobaric hypoxia, and it represents the initial cause of high-altitude illness (HAI). The physiology of HAI is discussed in more detail separately. (See "High-altitude illness: Physiology, risk factors, and general prevention", section on 'High altitude physiology'.)
PATIENT RISK ASSESSMENT AND MITIGATION
Risk factors — Risk factors for high-altitude illness (HAI) that are common to children and older patients include rapid rate of ascent, the absolute altitude achieved, the degree of physical exertion, cold weather, and history of prior HAI. (See "High-altitude illness: Physiology, risk factors, and general prevention", section on 'Risk factors'.)
Certain individuals develop high-altitude pulmonary edema (HAPE) upon repeated ascents above the same altitude and may, therefore, have an altitude threshold beyond which they are susceptible to HAPE. Individuals who have experienced multiple HAPE episodes in the past have demonstrated genetic or physiological susceptibility and are therefore at risk for recurrence with ascent to the same altitude and at the same rate. Recurrence in these individuals may be avoided with a slower rate of ascent or with pharmacologic prophylaxis.
Risk factors found more commonly in children include the following:
●Acute illness with upper or lower respiratory tract infection or other infection (eg, otitis media) [3-7]
●Congenital cardiopulmonary disease [8,9] (eg, unilateral absence of pulmonary artery) [10,11]; pulmonary hypertension [3]; cardiac shunts (atrial septal defect, ventricular septal defect, patent foramen ovale)
●Down syndrome, especially with obstructive sleep apnea [3,12]
●Systemic diseases that compromise respiratory function (eg, bronchopulmonary dysplasia [13], cystic fibrosis [14], sickle cell anemia [15], severe scoliosis [16], neuromuscular disease, obstructive sleep apnea)
●Full-term infants less than six weeks of age (premature infants less than 46 weeks post-conceptual age) [13,17]
●Premature and full-term infants who have experienced respiratory distress in the immediate postnatal period; infants up to one year of age with a history of oxygen requirement, bronchopulmonary dysplasia, or pulmonary hypertension [13,17]
●Susceptibility to re-ascent HAPE patient lives at high altitude [above 2500 m, 8200 feet], travels to low altitude for a short time period [eg, several days to weeks], and then returns home rapidly from low altitude) [18,19]
Recommendations for ascent — Healthy children should ascend to high altitudes slowly [20] and only if rapid descent is possible in the event of problems. Children have ascended safely as far as 15,580 to 18,040 feet (4570 to 5500 m). If the child has an acute upper respiratory infection, lower respiratory infection, or otitis media, extra caution should be exercised during rapid ascent above 2500 m (8200 feet) [20]. (See 'Risk factors' above.)
General measures to prevent HAI in children are derived from adult experience and include (see "High-altitude illness: Physiology, risk factors, and general prevention", section on 'Prevention of high-altitude illness'):
●Gradual ascent – Avoid abrupt ascent to sleeping altitudes above 2800 m (9200 feet).
●Acclimatization – Take measures to permit the child to become accustomed to higher altitudes:
•When ascending above 2500 m (8200 feet), do not spend subsequent nights at elevations more than 500 m higher than the previous night.
•Include a rest day (no ascent and no vigorous activity) for every 1000-m (3280-foot) increase in sleeping altitude.
•When possible, spend four to five days at an intermediate altitude (typically 3000 to 4000 m) before proceeding to higher elevations.
Recommendations for children with pre-existing illnesses — Infants and children with certain underlying diseases are at particular risk for significant complications, including exacerbation of their underlying condition or life-threatening high-altitude pulmonary edema (HAPE):
●Sickle cell disease – Patients with sickle cell disease who live at sea level should ascend cautiously if at all, as sickle cell crisis can occur at altitudes as low as 1500 m (4920 feet) [1]; symptoms are common at 2300 m (7544 feet). Patients with sickle cell trait may rarely become symptomatic from splenic sequestration or infarction at altitudes over 2500 m (8200 feet) [21-23].
●Asthma – Patients with asthma may find that their symptoms improve because of a relative lack of allergens at high altitudes. While theoretically bronchospasm induced by cold or exercise may worsen [24], patients with asthma appear to have no higher risk of altitude illness compared with those without asthma [21,25,26].
●Chronic lung disease – Children with chronic lung disease, such as cystic fibrosis or bronchopulmonary dysplasia, are at increased risk of significant hypoxemia and should undergo oxygen saturation monitoring during altitude travel. [27,28]. Again, ascent should be slow and cautious. One author suggests that children who are able to play and run without shortness of breath at home are unlikely to have problems lower than 3650 m (11,972 feet) [21]. Supplemental oxygen may enable other children to travel to altitudes between 2000 to 3000 m (6560 to 9840 feet) [26]. (See 'High-altitude pulmonary edema' below and "High-altitude pulmonary edema", section on 'Epidemiology and risk factors'.)
●Cardiac lesions with increased pulmonary artery blood flow – Infants and children with cardiac lesions involving an increase in pulmonary blood flow or pulmonary hypertension are at increased risk for HAPE. Isolated absence of the right pulmonary artery has been associated with development of HAPE at relatively low altitudes, and these patients should avoid exposure to high altitude [10,29]. Children with other cardiac defects that increase pulmonary flow, such as atrial and ventricular septal defects and patent ductus arteriosus, may be at increased risk for HAPE as well, and may benefit from oxygen saturation monitoring [25,30]. (See 'High-altitude pulmonary edema' below and "High-altitude pulmonary edema", section on 'Epidemiology and risk factors'.)
On the other hand, although an association has been reported between patent foramen ovale (PFO) and HAPE, causality is not established, and PFO is not considered a contraindication to high altitude exposure [31].
●Down syndrome – Children with trisomy 21 have increased pulmonary vascular reactivity and a higher risk of pulmonary hypertension in addition to an increased risk of congenital cardiac defects. They are also more likely to have obstructive sleep apnea and hypoventilation. These factors may be responsible for a higher risk of HAPE, even at relatively low altitudes [3]. Thus, travel to high altitude in children with trisomy 21 should be approached cautiously [25].
●Infants with a history of oxygen therapy or pulmonary hypertension – Infants under one year of age with a history of oxygen requirement or pulmonary hypertension have several unique physiologic limitations that place them at risk for hypoxemia, severe pulmonary hypertension, and, in extreme cases, right heart failure when rapidly exposed to high altitude (3000 to 5000 m [9840 to 16,400 feet]) [13,32]. (See 'Risk factors' above and 'High-altitude cerebral edema' below.)
HIGH-ALTITUDE ILLNESS IN CHILDREN
Acute mountain sickness (AMS) is the most common of the altitude illnesses. The risk of AMS depends upon individual susceptibility, the elevation reached, and the rate of ascent. Thus, while AMS is uncommon below 2000 m (6560 feet), it is quite common (approximately 25 percent incidence in adults and children) at sleeping elevations between 2000 and 3000 m (6560 to 9840 feet), where some cities and the majority of ski resorts in the Western United States are located (table 2 and table 1) [33-36]. In most instances, pediatric high-altitude illness (HAI) can be prevented with appropriate precautions or treated before serious illness, such as high-altitude pulmonary edema (HAPE) or high-altitude cerebral edema (HACE), occurs.
At higher altitudes, small observational studies initially suggested that AMS may occur more frequently in children and adolescents than in adults with ascent in a few hours from sea level to at elevations above 3500 m [33,37,38]. However, larger studies have found either the same incidence as adults or less:
●In one observational study that evaluated the impact of fast ascent among families with 157 children ascending 3450 m in 2.5 hours, AMS in children was lower (30 percent), compared with adolescents (37 percent) and adults (45 percent) [39]. In addition, familial clustering was consistent and explained 25 to 50 percent of variability, the first evidence of hereditary influence for AMS.
●In a separate study of 48 children who underwent the same rapid ascent profile, AMS incidence was 25 percent at 6 hours, 21 percent at 18 hours, and 8 percent at 42 hours; all AMS was mild, and none required descent [40].
●A third study took 118 children ages 6 to 16 in 2.5 hours to 3450 m in the Alps and found only a 6 percent incidence of AMS at 40 hours, confirming the rapid resolution of AMS without treatment [41].
Thus, the overall risk of AMS appears to be the same or less in children compared with adults, and as in adults, slower ascent rates reduce illness.
The epidemiology of AMS in adults is discussed in greater detail separately. (See "Acute mountain sickness and high-altitude cerebral edema", section on 'Epidemiology and Risk factors'.)
Acute mountain sickness — AMS and HACE are generally considered to represent two points along a single spectrum of disease, with the same underlying pathophysiology. Although some aspects of this pathophysiology remain unclear, the concept that AMS/HACE represents a continuum, and that AMS can progress to fatal HACE, fits with clinical experience and is helpful for management. However, especially in young children and infants, recognition of AMS is hampered by the difficulty in recognizing symptoms (eg, headache) in a nonverbal child. Certain pediatric patients (eg, infants under six weeks of age, children with congenital heart disease, cystic fibrosis, or Down syndrome) also have a greater susceptibility for life-threatening disease. (See 'Recommendations for children with pre-existing illnesses' above.)
Clinical manifestations — Signs of AMS in young children are nonspecific and include decreased playfulness, pallor, fussiness, poor sleep, vomiting, and decreased appetite [27,34,35].
In older children and adolescents, signs of HAI are similar to adults; the most common symptom is headache, which may be accompanied or followed by shortness of breath, dizziness, poor sleep, anorexia, fatigue, nausea, and vomiting [36]. The presentation and diagnosis of AMS in adults is discussed in greater detail separately. (See "Acute mountain sickness and high-altitude cerebral edema", section on 'Clinical features'.)
The onset of AMS is usually delayed for 6 to 12 hours following arrival at high altitude but can occur as rapidly as 1 to 2 hours or as late as 24 hours [42,43]. If there is no further ascent, symptoms are often most severe after the first night, generally resolve in one day with rest (eg, no skiing or hiking), and do not recur at the same altitude. AMS may reappear upon ascent to higher altitudes. On occasion, symptoms of AMS may persist for days despite no further ascent. In such cases, descent is required if there is no improvement with standard treatment. (See "Acute mountain sickness and high-altitude cerebral edema", section on 'AMS'.)
Supplemental oxygen may be used to support the clinical diagnosis of AMS. In our experience, providing 2 to 4 L/minute of oxygen by nasal cannula for 15 to 20 minutes prior to other interventions should markedly improve headache and other symptoms, as does a brief excursion to a lower altitude, especially in younger children.
The onset of symptoms more than two days after arrival at a given altitude, absence of headache, dyspnea at rest, and failure to improve rapidly with supplemental oxygen should prompt the clinician to search for an alternative diagnosis. No radiographic or laboratory testing is typically required unless the diagnosis of AMS is unclear. Other etiologies to consider include carbon monoxide poisoning, migraine (including new onset), dehydration, exhaustion, hyponatremia, viral syndrome, bacterial infection (eg, pneumonia or otitis), and occult trauma such as corneal abrasion. In young children, AMS is a diagnosis of exclusion.
AMS alone does not cause an elevation in body temperature, and an appropriate evaluation for fever based upon age and immunization status is warranted in febrile children at altitude. The clinician should pay close attention to the child's signs and response to oxygen, and when in doubt, should err on the side of a longer observation period before attributing symptoms to a condition other than AMS. (See "Fever without a source in children 3 to 36 months of age: Evaluation and management", section on 'Well-appearing patients'.)
Diagnosis — The diagnosis of AMS relies on typical clinical manifestations of vomiting, malaise, pallor, headache, fussiness, and/or difficulty breathing that occurs within 24 hours of arrival at high altitude without evidence of another cause (eg, otitis media, pneumonia, or viral illness). The diagnosis is supported by rapid improvement with supplemental oxygen or descent.
Treatment — The treatment of HAI in children follows the same principles as in adults [44]. All high-altitude illness responds to descent, although it is not always necessary. We find that a descent of 500 m (1600 ft) is sufficient for most children. It is important that group members and the afflicted individual remain alert for any symptoms or signs of worsening disease, particularly at elevations where AMS may rapidly progress to HACE (above 4000 m [13,120 feet]). (See "Acute mountain sickness and high-altitude cerebral edema", section on 'AMS' and "Acute mountain sickness and high-altitude cerebral edema", section on 'HACE'.)
Treatment of HAI is based upon symptom severity:
●Mild AMS – Mild AMS can be treated conservatively with symptomatic care (eg, acetaminophen or ibuprofen for headache, ondansetron for vomiting, rest, and fluid intake). Descent is not generally necessary.
●Moderate to severe AMS – Moderate/severe AMS (ie, AMS not resolving with rest or symptomatic care, or with moderate/severe symptoms) may require descent or supplemental oxygen (if available), and/or specific medication (table 3). Oxygen is most effective when used for a minimum of 2 to 4 hours, although we generally prescribe it for 12 to 24 hours, at a flow rate sufficient to maintain SpO2 at 90 to 92 percent (usually 1 to 2 L/minute). If oxygen is not available, and descent is delayed or impractical, dexamethasone should be administered, usually for 24 hours (table 3). Pediatric patients whose symptoms persist or worsen despite treatment must descend.
●HAPE – As with adults, treatment of HAPE requires descent and/or supplemental oxygen. (See 'High-altitude pulmonary edema' below.)
●HACE – In the exceedingly rare scenario of suspected pediatric HACE, immediate descent is indicated. Supplemental oxygen, dexamethasone, and hyperbaric therapy may temporize illness until evacuation is completed (table 3). (See "Acute mountain sickness and high-altitude cerebral edema", section on 'HACE'.)
Prevention and pharmacologic prophylaxis — Acclimatization and slow ascent are by far the best ways to avoid AMS. Travelers who ascend to high altitudes to ski, hike, or climb should be encouraged to limit their activity for the first few days at altitude. Adequate hydration is also important, although overhydration should be avoided to prevent hyponatremia.
To prevent AMS (and other altitude-related syndromes), experts recommend never traveling to (or sleeping at) 2750 m (9000 ft) or higher in one day from low altitude. In addition, individuals already above 2500 m (8200 feet) should not ascend to a sleeping altitude that is more than 500 m (1640 feet) above the previous night's altitude. This approach is particularly important for individuals who have experienced AMS or other altitude-related problems in previous ascents; such individuals are more likely to suffer from these disorders on subsequent exposure to high altitude. (See "High-altitude illness: Physiology, risk factors, and general prevention", section on 'Preacclimatization'.)
Acetazolamide prophylaxis — Prophylactic pharmacologic therapy with acetazolamide has not been studied in children who undergo rapid ascent. One prospective observational study of 48 older children and adolescents with rapid ascent to 3450 m found that 18 (38 percent) developed symptoms of AMS, but that no patient required specific pharmacologic treatment or evacuation to a lower altitude [40]. This study suggested that prophylactic therapy for AMS may be unnecessary in most healthy older children and adolescents who are not acclimatized.
If acetazolamide is used, the duration of treatment depends upon the ascent profile. Individuals ascending to a fixed sleeping altitude (eg, recreational skiers) may start acetazolamide the day before ascent and continue treatment for 48 hours. If further ascent is planned, acetazolamide can be continued until maximum elevation is attained. Acetazolamide can also be taken episodically to speed acclimatization at any point during altitude gain or to treat mild AMS. Symptoms do not recur when the drug is discontinued while at the same altitude. Although the danger of AMS passes after a few days of acclimatization, acetazolamide may still be useful for sleep. (See "Acute mountain sickness and high-altitude cerebral edema", section on 'Pharmacologic prevention of AMS/HACE' and "Acute mountain sickness and high-altitude cerebral edema", section on 'Preferred: acetazolamide'.)
The pediatric dose of acetazolamide for prevention of AMS is 1.25 mg/kg per dose twice a day (maximum single dose 125 mg) (table 3) [44]. The contraindication due to allergy to antibiotic sulfonamides has been challenged, and the risk of anaphylaxis from acetazolamide in such patients appears unlikely. On the other hand, a history of Stevens-Johnson reaction to an antibiotic sulfonamide is caused by a different mechanism than anaphylaxis, and some clinicians choose not to administer acetazolamide in these patients. (See "Sulfonamide hypersensitivity", section on 'Between sulfonamide antimicrobials and nonantimicrobials'.)
High-altitude cerebral edema — HACE is a rare life-threatening altitude disease that theoretically may occur in children [45]. In adults, HACE generally occurs in individuals with AMS and/or HAPE at elevations over 3000 to 3500 m (9840 to 11,480 feet) and is discussed in more detail separately. (See "Acute mountain sickness and high-altitude cerebral edema" and "High-altitude pulmonary edema", section on 'Epidemiology and risk factors'.)
High-altitude pulmonary edema — HAPE is a form of noncardiogenic pulmonary edema that may be fatal. In the United States, the incidence of HAPE in lowland children visiting high-altitude resorts in the Rocky Mountains is unknown. The overall incidence of HAPE is approximately 1 in 10,000 visitors, and many of these are children [46]. Three distinct forms of HAPE are described:
●Classic HAPE (cHAPE) – This form typically occurs in individuals ascending from low to high altitude, or individuals at high elevation rapidly ascending to higher elevation. cHAPE occurs among individuals who rapidly ascend to sleeping altitudes above 2500 m (8200 feet) [1], although altitude alone should not be used to exclude the diagnosis [46].
●Reentry HAPE (rHAPE) – This form is observed in high-altitude residents returning home from lower elevations.
●High-altitude resident pulmonary edema (HARPE) – This form is triggered in high-altitude residents by acute respiratory infection without altitude change.
As illustrated by the following studies, children who live at high altitudes and then temporarily descend are at risk for HAPE. Children with an acute viral upper respiratory tract infection who travel to or live at high altitude may have a slightly increased risk [4,5,18,28,47-49]:
●In a retrospective review of 39 episodes in 32 patients hospitalized for HAPE in Leadville, Colorado, the highest permanent community in the United States at an altitude of 10,152 feet (3094 m) above sea level, 25 of the 32 patients were under 15 years of age, and all but two victims were permanent residents of Leadville [18]. The majority of episodes followed a brief descent to lower altitudes; in three patients, the descent period was only 24 hours. A decrease in the incidence of HAPE was noted with increasing age, suggesting that an undefined response of the pediatric pulmonary vasculature to altitude may contribute to childhood frequency of HAPE.
●Similar childhood predominance of HAPE also was described in a study of 97 victims in the Andes; children between the ages of 2 and 12 years had more severe pulmonary edema than did older patients [49].
●An observational study reported cardiac catheterization results for seven children who lived in Leadville, Colorado and who had recovered from HAPE [4]. Three children had HAPE in association with a viral upper respiratory tract infection without any prior descent. These patients had a greater mean pulmonary artery pressure in response to hypoxia.
●Upper respiratory infection (colds, bronchitis, or otitis media) in the period immediately preceding ascent also appears to predispose children who live at low altitude to development of HAPE; this phenomenon may be related to the release of inflammatory mediators during infection [5]. Furthermore, children have greater pulmonary vascular reactivity than adults, and inflammation increases capillary permeability. Together, these cause proportionally more pulmonary edema in children.
Clinical manifestations — In young children, HAPE presents as increasing respiratory distress over one to two days, but may develop more precipitously. Young children and infants may manifest only pallor and depressed consciousness or other nonspecific symptoms such as increased fussiness, crying, decreased appetite, decreased playfulness, disrupted sleep, and possibly vomiting [6,25,34,35]. In infants, increased pulmonary artery pressure and fetal shunting, with or without HAPE, can cause severe hypoxemia. Thus, the pulse oximetry may be low relative to normal values at that altitude. The table provides mean values and range of normal values for arterial blood gas results and oxygen saturation at different altitudes and by exposure to assist with interpretation (table 4). (See "High-altitude pulmonary edema", section on 'Pathophysiology'.)
In older children and adolescents, HAPE may present as an insidious cough, fatigue, breathlessness out of proportion to work, breathlessness at rest, and production of frothy, often rusty, sputum. Physical findings at this time include rapid breathing, cyanosis, tachycardia, and diffuse crackles on lung auscultation. When available, a chest radiograph reveals diffuse interstitial changes typical of noncardiogenic pulmonary edema. (See "Noncardiogenic pulmonary edema".)
HAPE may appear over the course of several hours or days, but may also present explosively. It is most common after two nights at a high altitude. It can occur without preceding AMS.
Elevation in body temperature over 38.3°C from HAPE alone is unusual; higher temperatures warrant evaluation for a concurrent infection or another diagnosis. Young children with a higher fever should be assessed based upon age and immunization status. However, respiratory infection and HAPE can coexist. (See "Fever without a source in children 3 to 36 months of age: Evaluation and management", section on 'Well-appearing patients'.)
The differential diagnosis in children includes pneumonia, heart failure, and other forms of non-cardiogenic pulmonary edema. (See "Pathophysiology of left-to-right shunts" and "Isolated ventricular septal defects (VSDs) in infants and children: Anatomy, clinical features, and diagnosis" and "Isolated atrial septal defects (ASDs) in children: Classification, clinical features, and diagnosis" and "Community-acquired pneumonia (CAP) in children: Clinical features and diagnosis", section on 'Clinical presentation'.)
Diagnosis — The diagnosis of HAPE relies on typical clinical manifestations of cough, fatigue, dyspnea, frothy sputum, diffuse crackles on auscultation of the lungs, respiratory distress, and/or hypoxemia for the specific altitude (table 4) that present one to two days after high altitude exposure without evidence of another cause (eg, pneumonia). In infants and young children, HAPE may be accompanied by other nonspecific signs of AMS such as fussiness, decreased activity, decreased appetite, and vomiting. If performed, chest radiographs show diffuse interstitial changes consistent with noncardiogenic pulmonary edema.
Laboratory findings may include leukocytosis (likely from the stress response to hypobaric hypoxia), and elevated C-reactive protein; these may lead clinicians to consider treatment for concomitant infectious processes [50-52]. Additionally, mild increases in B-type natriuretic peptide and troponin may be seen and generally normalize rapidly with resolution of illness.
Treatment — The treatment of HAPE in lowland children who ascend to high altitude targets the same goal as in older patients: the prompt reduction of pulmonary artery (PA) pressure and hypoxemia via increasing the partial pressure of inspired oxygen [44,53].
Options include:
●Limiting physical exertion and cold exposure
●Providing supplemental oxygen via tank or concentrator
●Evacuation to a lower altitude
●Simulating descent using hyperbaric therapy
●Nifedipine (≥50 kg) or amlodipine (<50 kg or <17 years old) (table 3)
Of these treatments, descent (simulated or actual) and/or supplemental oxygen are most often effective alone and appear to be superior to any pharmacologic therapy. In some resort areas, children with HAPE are treated as outpatients with supplemental oxygen and remain at the same altitude with their families with close follow-up. Nifedipine or amlodipine have also been suggested (table 3) [25,46,53]. Compared with nifedipine, amlodipine offers advantages for small children because of once-daily dosing and availability as liquid or appropriately sized tablets. (See "High-altitude pulmonary edema", section on 'Treatment'.)
Inappropriate use of antibiotics and diuretics in children with HAPE is not efficacious and should be discouraged [46].
For severely ill children, especially those with impaired consciousness, supplemental oxygen by high-flow nasal canula or noninvasive ventilation may be necessary. Tracheal intubation is rarely required. Notably, it can take one to two hours for noticeable improvement and reduction in oxygen requirement in severe illness.
A small proportion of children with HAPE may have an underlying predisposing condition. In one study, 17 percent of children with HAPE who underwent echocardiogram were diagnosed with new structural heart findings (eg, patent foramen ovale [PFO] and atrial septal defects [ASDs]) [46]. Thus, an echocardiogram is warranted to evaluate for underlying pulmonary hypertension and to rule out structural abnormalities that are known risk factors, such as an ASD, isolated pulmonary artery of ductal origin, coarctation of the aorta, ventriculoseptal defect, and pulmonary vein stenosis [30,46]. A PFO may be a risk factor, depending on its size.
Prevention — As with AMS, slow ascent is the best method to prevent HAPE. Individuals with previous HAPE should be encouraged to ascend slowly and be prepared to descend quickly if symptoms of HAPE appear. (See "High-altitude pulmonary edema", section on 'Prevention'.)
For healthy children residing at low altitude and without a history of HAPE, we recommend adequate acclimatization and do not use pharmacologic HAPE prophylaxis. Some experts have suggested using nifedipine or amlodipine for prevention of HAPE in susceptible children based on adult data and class effect [53]. However, calcium channel blockers have not been studied specifically in children for HAPE prophylaxis. Nifedipine is the preferred drug for the prevention of HAPE in susceptible adults, but the commonly available nifedipine formulations contain inappropriately large doses for children [26]. In the rare circumstance that a child has had past episodes of HAPE and slow ascent is not possible, prophylaxis with amlodipine would be a reasonable option. The dose is 2.5 to 5 mg orally once daily (child 6 to 17 years old and ≥25 kg) or 0.1 to 0.6 mg/kg/dose orally once daily (maximum 5 mg/day; child 1 to 5 years old or <25 kg). Ideally, prophylaxis is started 24 hours prior to ascent and continued for five days at the destination altitude (table 3). In higher-risk scenarios, treatment may be continued for a longer period. (See "High-altitude pulmonary edema", section on 'Prophylactic medications'.)
Experience among clinicians in Colorado suggests that acetazolamide prophylaxis for children with recurrent re-entry HAPE may be effective (table 3). Although this has not been formally studied, acetazolamide is known to reduce pulmonary artery pressure on ascent to altitude as well as speed acclimatization. Some experts recommend a lower prophylactic dose (1.25 mg/kg instead of 2.5 mg/kg, both twice daily). However, this lower dose is based on adult studies, and we do not suggest its use until further pediatric-specific data are available.
Other altitude-related illness — High-altitude retinal hemorrhage and high-altitude periodic breathing of sleep are other types of altitude illness that may occur in children. In addition, children are more prone to hypothermia because of the larger surface area to mass ratio and the decreased glycogen stores available for increased energy needs in cold weather. Young children are also prone to frostbite if proper attention to appropriate clothing and limitation of cold exposure is not provided by caregivers. (See "Hypothermia in children: Clinical manifestations and diagnosis", section on 'Pediatric considerations' and "Frostbite: Acute care and prevention", section on 'Risk factors'.)
High-altitude pulmonary hypertension — Serious high-altitude pulmonary hypertension (HAPH) is rare in healthy infants and children. However, infants less than six weeks of age are at particular risk for pulmonary hypertension and progression to right heart failure [54]. This entity has been described in up to 1 percent of infants of lowland parents who are born or arrive at high altitude (3000 to 5000 m [9840 to 16,400 feet]) and remain there for more than a month; it occurs almost exclusively in this group [25]. Because of the risk of this disorder, exposure to prolonged high altitude should be avoided in infants younger than six weeks of age who normally live at low altitude or whose gestation primarily occurred at low altitude [32].
Infants between six weeks and one year of age may have a higher incidence of pulmonary hypertension with hypoxia, patent ductus arteriosus (PDA), and PFO with prolonged exposure to high altitudes [13,55]. Those infants who will be remaining indefinitely at altitude warrant physical examination and an initial measurement of pulse oximetry followed by regular monitoring at well child visits. Patients with physical findings suggesting pulmonary hypertension (eg, systolic ejection murmur with a single or narrowly split second heart sound) or other structural heart disease should have an electrocardiogram. An echocardiogram is also necessary if clinical findings suggest structural heart disease or pulmonary hypertension. (See "Pulmonary hypertension in children: Classification, evaluation, and diagnosis", section on 'Evaluation'.)
High-altitude retinal hemorrhage — High-altitude retinal hemorrhage (HARH) is a relatively common finding at altitudes above 4270 m (14,005 feet), but it usually is asymptomatic and thus, unrecognized unless the macula is involved. The usual complaint is blurring of vision and funduscopy shows flame-like retinal hemorrhages. As with all other forms of altitude disease, slow ascent is preventive, and descent is the best treatment. No medications have been found to prevent or treat HARH. Any individual with hemorrhage affecting vision should descend. The retinal hemorrhages resolve slowly over the course of several weeks to months. (See "High-altitude illness: Physiology, risk factors, and general prevention", section on 'Other altitude-related illnesses'.)
High-altitude periodic breathing of sleep — Periodic breathing of sleep at high altitude is a form of Cheyne-Stokes respiration that occurs almost exclusively during non-REM sleep and can awaken subjects if the hyperventilation phase is strong enough. Children may be less disposed to this problem than adults. As an example, an observational study of 20 children between 9 and 12 years of age and their fathers which compared respiratory inductive plethysmography, pulse oximetry, and end-tidal CO2 measurements during sleep at 3450 m (11,316 feet) versus 490 m (1607 feet), children were noted to have markedly less periodic breathing but similar hyperventilation and decrease in nocturnal oxygen saturation compared with adults [33]. Furthermore, 50 percent of children met criteria for AMS versus 30 percent of adults during the course of the study. This finding suggests that the more stable breathing pattern displayed by these children is related to a lower apnea threshold for CO2 and does not render them more tolerant of high altitude. (See "High-altitude illness: Physiology, risk factors, and general prevention", section on 'Other altitude-related illnesses'.)
TRAVEL ADVICE FOR PARENTS/CAREGIVERS
Healthy infants and children — Healthy infants over six weeks of age and young children, including those with well-controlled asthma, typically tolerate travel to altitude well and rarely experience any serious high-altitude illness (HAI).
Clinicians should discourage high altitude travel for infants under six weeks of age who were born at or whose gestations was primarily at low elevation (<1500 m [4920 feet]) because they are at risk for abrupt severe hypoxemia, pulmonary hypertension, and right-sided heart failure. (See 'Risk factors' above and 'High-altitude cerebral edema' above.)
The following measures reduce the risk or enable easy management of HAI in young children [17]:
●Gradual ascent – As a general guideline, individuals who normally reside below 1500 m (4920 feet) elevation must avoid an abrupt ascent to sleeping altitudes above 2750 m (9000 feet). This is best accomplished by spending one night at an intermediate altitude, such as 1600 to 2200 m (particularly when traveling to an elevation that caused symptoms previously). Two nights is even better. (See 'Prevention and pharmacologic prophylaxis' above and "High-altitude illness: Physiology, risk factors, and general prevention", section on 'Gradual or staged ascent'.)
●Avoid overexertion the first two days – Strenuous hiking, skiing, etc, should only follow one to two days of acclimatization. If exertion is unavoidable, such as backpacking that requires carrying a heavy pack, ascent needs to be even slower.
●Acetazolamide prophylaxis – Most experts do not routinely prescribe acetazolamide prophylaxis in otherwise healthy children or adults who are gradually ascending to high altitudes [1]. Prophylaxis may be indicated in situations where gradual ascent is not possible (eg, rapid ascent by airplane to a destination above 2750 m [9000 feet]) and in children who have had repeated episodes of acute mountain sickness (AMS) when previously exposed to a similar altitude and rate of ascent. However, a past history of AMS in children is an unreliable predictor of repeat illness [56]. (See 'Acetazolamide prophylaxis' above.)
●Symptomatic treatment – Parents or other caregivers should travel with ibuprofen. The appropriate dose of ibuprofen can quickly improve fussiness in young children or alleviate headaches in older children.
Ondansetron may also be prescribed for use as necessary, especially if the patient is sleeping over 9000 feet or is participating in a long trek.
●Availability of descent – Descent from altitude should be readily available if serious HAI occurs. Destinations for which rapid descent is difficult require caution and planning.
●Medical resources – Resort communities generally have health care providers with expertise in HAI who are excellent resources for parents or other caregivers. If HAI is diagnosed in these settings, it can usually be managed so that the trip can continue.
Clinicians should counsel caregivers to assess emergency rescue or medical care capabilities in remote settings relative to the risk of HAI in their children.
With proper education, most parents and caregivers can recognize risk factors and symptoms and signs of HAI, even in preverbal children [35]. This knowledge can help caregivers decide when AMS is likely the problem, and how to respond as described above [17]. (See 'Acute mountain sickness' above.)
Caregivers should also know to seek immediate medical attention for altered mental status such as marked drowsiness, respiratory distress, or ataxia. (See 'High-altitude cerebral edema' above and 'High-altitude pulmonary edema' above.)
Children who develop mild AMS that resolves with descent or medication do not require specific evaluation [17].
Children who normally reside at altitude and manifest severe hypoxemia or high-altitude pulmonary edema (HAPE) warrant an evaluation for pulmonary hypertension or structural cardiac abnormality [4,9].
Susceptible infants and children — Parents or other caregivers of children with the following conditions should be advised to avoid travel to high altitude [13,17] (see 'Risk factors' above):
●Full-term infants less than six weeks of age (premature infants less than 46 weeks postconceptual age) or full-term infants up to one year of age with a history of oxygen requirement or pulmonary hypertension
●Premature infants beyond 46 weeks post-conceptual age with a history of oxygen requirement, bronchopulmonary dysplasia, or pulmonary hypertension
●Congenital heart disease with pulmonary hypertension, cyanosis, or intracardiac shunts
●Sickle cell disease
●Down syndrome with cardiac shunts or pulmonary hypertension
●Active respiratory disease such as pneumonia, bronchiolitis, or cystic fibrosis with exacerbation
Children with stable cystic fibrosis may be able to travel to high altitude if pulse oximetry monitoring is performed during travel and supplemental oxygen can be provided. Assessment of FEV1 and hypoxia inhalation testing can be performed in children over six years of age and can help identify those children who warrant supplemental oxygen during the trip [26]. Almost all resort areas have home oxygen companies that honor prescriptions for oxygen written by licensed providers. Caregivers should ensure strict adherence to established chest physiotherapy, mucolytic, and antibiotic regimens during the trip.
Children with neuromuscular disorders or conditions causing restrictive lung disease (eg, severe kyphoscoliosis) should undergo assessment by a pediatric pulmonologist prior to travel to determine the need for supportive measures while at high altitude, such as supplemental oxygen (continuous or nocturnal) or nighttime bilevel positive airway pressure [26].
INFORMATION FOR PATIENTS
UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topic (see "Patient education: High-altitude illness (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Altitude and risk for high-altitude illness (HAI) – The risk of HAI depends upon individual susceptibility, the rate of ascent, and the elevation reached. Ascent above 2500 m (8200 feet) may be associated with HAI in children. However, most healthy children do well without any serious effects at altitudes less than 3500 m (11,480 feet). (See 'High-altitude illness in children' above.)
●Risk factors for HAI – Children at particular risk for serious HAI include the following (see 'Risk factors' above and 'High-altitude cerebral edema' above and 'High-altitude pulmonary hypertension' above):
•Infants under six weeks of age
•Infants up to one year of age with a history of oxygen requirement or pulmonary hypertension, including premature infants
•Children who live at very high altitude and undergo a temporary descent
•Children with Down syndrome, congenital heart disease, cystic fibrosis or neuromuscular problems compromising ventilation
●Acute mountain sickness (AMS)
•Clinical manifestations – Clinical manifestations of AMS are nonspecific in young children and infants and include decreased playfulness, pallor, fussiness, poor sleep, vomiting, and decreased appetite (table 5). A high index of suspicion is required for detection. (See 'Clinical manifestations' above.)
Symptoms of AMS in older children and adolescents are similar to those seen in adults. The most common symptom is headache, which may be accompanied or followed by shortness of breath, dizziness, poor sleep, anorexia, fatigue, nausea, and vomiting. (See "Acute mountain sickness and high-altitude cerebral edema", section on 'Clinical features'.)
•Diagnosis – The diagnosis of AMS relies on typical clinical manifestations that occur within 24 hours of arrival at high altitude without evidence of another cause (eg, otitis media, pneumonia, or viral illness). AMS is a diagnosis of exclusion in preverbal children. Improvement of symptoms after administration of supplemental oxygen (eg, 2 to 4 L/minute by nasal cannula for 15 to 20 minutes) or a brief descent supports the diagnosis of AMS if no other cause is found. (See 'Diagnosis' above.)
•Treatment – Children with AMS are treated based upon symptom severity following the same principles as in adults (table 3). (See 'Treatment' above.)
●High-altitude pulmonary edema (HAPE)
•Clinical manifestations – Although rare in young children, HAPE presents as increasing respiratory distress over one to two days, but may develop more precipitously. In some young children and infants, primary signs may not include tachypnea, but oxygen saturation will always be low relative to normal values at that altitude (table 4). Symptoms of HAPE in older children and adolescents are similar to those in adults: dyspnea, tachypnea, rales, and cough productive of frothy, rusty sputum. (See 'Clinical manifestations' above.)
•Diagnosis – The diagnosis of HAPE relies on typical clinical manifestations that present one to two days after high-altitude exposure without evidence of another cause (eg, pneumonia). If performed, chest radiographs show diffuse interstitial changes consistent with noncardiogenic pulmonary edema. (See 'Diagnosis' above.)
•Treatment – Children with HAPE warrant immediate supplemental oxygen, descent or both. In emergency settings without the option of oxygen or descent, pharmacotherapy with nifedipine (≥50 kg) or amlodipine (<50 kg or <17 years old) may be effective (table 3). (See 'Treatment' above.)
●Prevention of AMS and HAPE – Acclimatization and slow ascent are the most effective ways to avoid AMS and HAPE in otherwise healthy children. (See 'Prevention and pharmacologic prophylaxis' above and 'Prevention' above.)
Healthy children should ascend to very high altitudes (over 3500 m [11,480 feet]) slowly and only if rapid descent is possible in the event of problems. (See 'Recommendations for ascent' above.)
●Travel advice for parents/caregivers – Healthy children generally tolerate travel to altitude well and rarely experience any serious HAI. The clinician should advise parents or other caregivers that resort communities generally have health care providers with expertise in altitude-related problems who are excellent resources if they feel their child might be experiencing HAI
高海拔生理學
在高海拔地區，吸入氧分壓 (PIO2) 降低是氣壓降低的直接結果。隨著 PIO2 的降低，肺泡氧分壓 (PAO2)、動脈血氧分壓 (PaO2) 和動脈血氧飽和度 (SpO2) 也隨之降低，導致組織缺氧。這種缺氧形式被稱為低壓性缺氧，是高海拔疾病 (HAI) 的初始原因。
患者風險評估與緩解
風險因子 － 兒童和老年患者常見的HAI風險因子包括上升速度過快、達到的絕對海拔高度、體力消耗程度、寒冷天氣以及過去的高海拔疾病史。
風險因子 － 兒童和老年患者常見的HAI風險因子包括上升速度過快、達到的絕對海拔高度、體力消耗程度、寒冷天氣以及過去的高海拔疾病史。
某些人在反覆攀登同一海拔高度後會發生高海拔肺水腫（HAPE），因此可能存在一個海拔閾值，超過該閾值他們就容易發生HAPE。過去多次發生HAPE的個體表示有遺傳或生理易感性，因此以相同速度攀登至相同海拔高度時，他們有復發的風險。對於這些個體，可以透過降低攀登速度或進行藥物預防來避免復發。
兒童常見的危險因子包括以下幾點：
●急性疾病，伴隨上呼吸道或下呼吸道感染或其他感染（例如，中耳炎）[ 3-7 ]
●先天性心肺疾病[ 8,9 ]（例如，單側肺動脈缺如）[ 10,11 ]；肺動脈高壓[ 3 ]；心臟分流（心房中隔缺損、心室中隔缺損、卵圓孔未閉）
●唐氏症，尤其是伴隨阻塞性睡眠呼吸中止症[ 3,12 ]
●損害呼吸功能的全身性疾病（例如，支氣管肺發育不良[ 13 ]、囊性纖維化[ 14 ]、鐮狀細胞貧血[ 15 ]、嚴重脊椎側彎[ 16 ]、神經肌肉疾病、阻塞性睡眠呼吸中止症）
●足月嬰兒，出生不足六週（早產兒，出生後46週）[ 13,17 ]
●早產兒和足月兒在出生後立即出現呼吸窘迫；一歲以下有吸氧史、支氣管肺發育不良或肺動脈高壓的嬰兒[ 13,17 ]
●HAPE 患者容易再次發生高山症（HAPE 患者居住在高海拔地區 [2500 米，8200 英尺以上]，在低海拔地區短期旅行 [例如，幾天到幾週]，然後迅速從低海拔地區返回家中）[ 18,19 ] 。
攀登建議 － 健康兒童應緩慢攀登至高海拔地區[ 20 ]，且僅在出現問題時能夠迅速下降的情況下方可攀登。兒童已安全攀登至海拔 4570 至 5500 公尺（15580 至 18040 英尺）。若兒童患有急性上呼吸道感染、下呼吸道感染或中耳炎，則在海拔 2500 公尺（8200 英尺）以上快速攀登時應格外謹慎[ 20 ]。
預防兒童高山症的一般措施源於成人的經驗，包括：
●逐漸上升－避免突然上升到海拔 2800 公尺（9200 英尺）以上的睡眠海拔。
●適應性訓練－採取措施讓孩子逐漸適應高海拔地區：
•當海拔上升到 2500 公尺（8200 英尺）以上時，不要在比前一晚高出 500 公尺以上的海拔過夜。
•每增加 1000 公尺（3280 英尺）的睡眠海拔，就應安排一天休息日（不進行攀登和劇烈活動）。
•如果條件允許，在前往更高海拔地區之前，先在中等海拔地區（通常為 3000 至 4000 公尺）停留四到五天
對患有潛在疾病的兒童的建議 － 患有某些潛在疾病的嬰幼兒尤其容易出現嚴重的併發症，包括潛在疾病加重或危及生命的高海拔肺水腫（HAPE）：
●鐮狀細胞疾病－居住在海平面的鐮狀細胞疾病患者應謹慎登山，甚至最好不要登山，因為鐮狀細胞危象可能發生在海拔低至 1500 公尺（4920 英尺）的地方[ 1 ]；症狀在海拔 2300 公尺（7544 英尺）處較為常見。鐮狀細胞性狀攜帶者在海拔 2500 公尺（8200 英尺）以上的地方極少數情況下可能因脾臟滯留或梗塞而出現症狀[ 21-23 ]。
●氣喘－氣喘患者可能會發現，由於高海拔地區過敏原相對較少，他們的症狀會有所改善。雖然理論上由寒冷或運動引起的支氣管痙攣可能會加重[ 24 ]，但與非氣喘患者相比，氣喘患者發生高山症的風險似乎並沒有增加[ 21,25,26 ]。
●慢性肺部疾病－患有慢性肺部疾病（例如囊性纖維化或支氣管肺發育不良）的兒童發生嚴重低氧血症的風險較高，因此在高海拔旅行期間應進行氧飽和度監測。 [ 27,28 ] 再次強調，攀登應緩慢謹慎。一位作者指出，在家中能夠自由玩耍奔跑而不出現呼吸困難的兒童，在海拔低於3650公尺（11972英尺）的地方不太可能出現問題。 [ 21 ] 補充氧氣可能使其他兒童能夠前往海拔2000至3000公尺（6560至9840英尺）之間的地區。 [ 26 ]
預防兒童高山症的一般措施源於成人的經驗，包括：
●逐漸上升－避免突然上升到海拔 2800 公尺（9200 英尺）以上的睡眠海拔。
●適應性訓練－採取措施讓孩子逐漸適應高海拔地區：
•當海拔上升到 2500 公尺（8200 英尺）以上時，不要在比前一晚高出 500 公尺以上的海拔過夜。
•每增加 1000 公尺（3280 英尺）的睡眠海拔，就應安排一天休息日（不進行攀登和劇烈活動）。
•如果條件允許，在前往更高海拔地區之前，先在中等海拔地區（通常為 3000 至 4000 公尺）停留四到五天
對患有潛在疾病的兒童的建議 － 患有某些潛在疾病的嬰幼兒尤其容易出現嚴重的併發症，包括潛在疾病加重或危及生命的高海拔肺水腫（HAPE）：
●鐮狀細胞疾病－居住在海平面的鐮狀細胞疾病患者應謹慎登山，甚至最好不要登山，因為鐮狀細胞危象可能發生在海拔低至 1500 公尺（4920 英尺）的地方[ 1 ]；症狀在海拔 2300 公尺（7544 英尺）處較為常見。鐮狀細胞性狀攜帶者在海拔 2500 公尺（8200 英尺）以上的地方極少數情況下可能因脾臟滯留或梗塞而出現症狀[ 21-23 ]。
●氣喘－氣喘患者可能會發現，由於高海拔地區過敏原相對較少，他們的症狀會有所改善。雖然理論上由寒冷或運動引起的支氣管痙攣可能會加重[ 24 ]，但與非氣喘患者相比，氣喘患者發生高山症的風險似乎並沒有增加[ 21,25,26 ]。
●慢性肺部疾病－患有慢性肺部疾病（例如囊性纖維化或支氣管肺發育不良）的兒童發生嚴重低氧血症的風險較高，因此在高海拔旅行期間應進行氧飽和度監測。 [ 27,28 ] 再次強調，攀登應緩慢謹慎。一位作者指出，在家中能夠自由玩耍奔跑而不出現呼吸困難的兒童，在海拔低於3650公尺（11972英尺）的地方不太可能出現問題。 [ 21 ] 補充氧氣可能使其他兒童能夠前往海拔2000至3000公尺（6560至9840英尺）之間的地區。 [ 26 ]
伴隨肺動脈血流量增加的心臟病變－患有伴隨肺動脈血流量增加或肺動脈高壓的心臟病變的嬰幼兒發生高海拔肺水腫的風險增加。右肺動脈孤立性缺如與在相對低海拔地區發生高海拔肺水腫有關，這些患者應避免暴露於高海拔地區[ 10,29 ]。其他可增加肺血流量的心臟缺陷，例如房間隔缺損、室間隔缺損和動脈導管未閉，也可能增加發生高海拔肺水腫的風險，並可能受益於氧飽和度監測[ 25,30 ]。
另一方面，雖然有報告指出卵圓孔未閉 (PFO) 與 HAPE 之間存在關聯，但因果關係尚未確定，PFO 也不被認為是高海拔暴露的禁忌症
唐氏症－21三體症兒童除了先天性心臟缺陷風險增加外，肺血管反應性增強，肺動脈高壓風險也較高。他們也更容易出現阻塞性睡眠呼吸中止症和通氣不足。這些因素可能導致即使在相對較低的海拔，他們發生高海拔肺水腫（HAPE）的風險也更高[ 3 ]。因此，對於21三體症患兒，應謹慎安排高海拔旅行[ 25 ]。
●有氧療史或肺動脈高壓史的嬰兒－1歲以下有氧療史或肺動脈高壓史的嬰兒存在一些獨特的生理限制，使他們在快速暴露於高海拔（3000至5000米[9840至16400英尺]）時，容易發生低氧血症、嚴重肺動脈高壓，在極端情況下會發生右心衰竭
兒童AMS
AMS是最常見的高山症。 AMS的風險取決於個體的易感性、到達的海拔高度以及上升速度。因此，雖然在海拔2000米（6560英尺）以下AMS並不常見，但在海拔2000米至3000米（6560至9840英尺）的睡眠海拔範圍內，AMS卻相當常見（成人和兒童的發病率約為25%），而美國西部的一些城市和大多數滑雪勝地就位於這一海拔高度（表 3-32） [323-36] 3-366 ] 3-3623-36213-323-32713-3276 7607年）。在大多數情況下，可以透過適當的預防措施來預防兒童HAI，或在出現嚴重疾病（例如HAPE或HACE前進行治療。
在高海拔地區，一些小型觀察性研究最初表明，兒童和青少年在數小時內從海平面上升到海拔3500公尺以上時，發生急性高山症的頻率可能高於成人[ 33,37,38 ]。然而，更大規模的研究發現，兒童和青少年發生急性高山症的頻率與成人相同或更低：
●一項觀察性研究評估了快速攀登對家庭的影響，該研究納入了157名兒童，他們在2.5小時內攀登了3450公尺。結果顯示，兒童發生急性高山症（AMS）的比例（30%）低於青少年（37%）和成人（45%）[ 39 ]。此外，家族聚集性表現穩定，可解釋25%至50%的變異性，這是AMS遺傳影響的首個證據。
●在另一項針對 48 名接受相同快速上升方案的兒童的研究中，6 小時時急性高山症發生率為 25%，18 小時時為 21%，42 小時時為 8%；所有急性高山症均為輕度，且均無需下降 [ 40 ]。
●第三項研究讓 118 名 6 至 16 歲的兒童在 2.5 小時內到達阿爾卑斯山 3450 公尺的高度，結果發現 40 小時內僅有 6% 的兒童出現急性高山症，證實了急性高山症無需治療即可迅速緩解 [ 41 ]。
因此，兒童急性高山症的整體風險似乎與成人相同或更低，而且與成人一樣，較慢的上升速度可以降低罹病風險。
成人急性高山症的流行病學將在另一章節中進行更詳細的討論。 （請參閱 「急性高山症與高海拔腦水腫」章節中的「流行病學與危險因子」部分。）
急性高山症 （ AMS）和高海拔腦水腫（HACE）通常被認為是同一疾病譜上的兩個階段，具有相同的潛在病理生理機制。儘管這種病理生理機制的某些方面仍不清楚，但AMS/HACE代表一個連續光譜，並且AMS可發展為致命的HACE這一概念符合臨床經驗，有助於疾病管理。然而，尤其是在幼兒和嬰兒中，由於難以識別非語言兒童的症狀（例如頭痛），AMS的識別受到阻礙。某些兒科患者（例如，6週齡以下的嬰兒、患有先天性心臟病、囊性纖維化或唐氏症的兒童）也更容易患上危及生命的疾病。 （請參閱上文「針對患有既往疾病的兒童的建議」。）
臨床表現 － 幼兒急性代謝症候群的症狀不具特異性，包括玩耍減少、臉色蒼白、煩躁不安、睡眠品質差、嘔吐和食慾下降[ 27,34,35 ]。
在年齡較大的兒童和青少年中，高山症的症狀與成人相似；最常見的症狀是頭痛，可能伴隨或隨後出現呼吸困難、頭暈、睡眠品質差、厭食、疲勞、噁心和嘔吐[ 36 ]。成人急性高山症的臨床表現和診斷將在其他章節中詳細討論。 （請參閱 「急性高山症與高海拔腦水腫」章節中的「臨床特徵」部分。）
急性高山症通常在到達高海拔地區後6至12小時出現，但也可能在1至2小時內或24小時後出現[ 42,43 ]。如果沒有進一步上升，症狀通常在第一個晚上最為嚴重，休息一天後（例如，停止滑雪或遠足）一般會緩解，並且不會在同一海拔高度復發。但上升到更高海拔時，急性高山症可能會再次出現。有時，即使沒有進一步上升，急性高山症的症狀也可能持續數天。在這種情況下，如果標準治療無效，則需要下降。 （請參閱 「急性高山症與高海拔腦水腫」章節中的「急性高山症」部分。）
補充氧氣可用於輔助急性高山症的臨床診斷。根據我們的經驗，在採取其他幹預措施之前，透過鼻導管以 2 至 4 公升/分鐘的流量給予氧氣 15 至 20 分鐘，可顯著改善頭痛和其他症狀；短暫下到較低海拔地區也有類似效果，尤其對年幼兒童而言。
如果症狀在到達特定海拔高度兩天後才出現，且無頭痛、靜止時呼吸困難，以及吸氧後症狀未迅速改善，則臨床醫生應考慮其他診斷。除非急性高山症的診斷不明確，否則通常無需進行影像學或實驗室檢查。其他需要考慮的原因包括一氧化碳中毒、偏頭痛（包括新發偏頭痛）、脫水、疲勞、低鈉血症、病毒感染、細菌感染（如肺炎或中耳炎）以及隱性外傷，例如角膜擦傷。在幼兒中，急性高山症的診斷是一種排除性診斷。
單純的急性高山症不會導致體溫升高，因此，對於在高地地區出現發燒症狀的兒童，應根據其年齡和免疫接種情況進行適當的發燒評估。臨床醫師應密切觀察兒童的徵兆和對氧氣的反應，如有疑問，應傾向於延長觀察期，然後再將症狀歸因於急性高山症以外的其他疾病。 （請參閱 “3至36個月大兒童不明原因發燒：評估和處理”，其中“外觀良好的患者”部分。）
診斷 － 急性高山症的診斷主要依據典型的臨床表現，包括嘔吐、疲倦、蒼白、頭痛、煩躁不安和/或呼吸困難，這些症狀通常在抵達高海拔地區後24小時內出現，且排除其他病因（例如中耳炎、肺炎或病毒感染）。吸氧或下降海拔後症狀迅速改善可支持診斷。
治療 － 兒童高山症的治療原則與成人相同[ 44 ]。所有高山反應都會隨著下降而緩解，儘管並非總是必須下降。我們發現，下降500公尺（1600英尺）對大多數兒童來說就足夠了。重要的是，團隊成員和患者本人要時刻警惕任何症狀或病情惡化的跡象，尤其是在海拔4000公尺（13120英尺）以上，因為急性高山症可能迅速發展為高山腦水腫（HACE）。
院內獲得性感染的治療取決於症狀的嚴重程度：
●輕度高山症－輕度高山症可採用保守治療，包括症狀治療（例如，服用乙醯胺酚或布洛芬緩解頭痛，服用昂丹司瓊緩解嘔吐，以及休息和補充水分）。通常無需下降。
●中重度急性高山症－中重度急性高山症（即休息或對症治療無效，或症狀為中重度）可能需要下山或吸氧（如有條件），和/或使用特定藥物（表3）。吸氧至少2至4小時效果最佳，但我們通常建議吸氧12至24小時，氧流量應足以維持血氧飽和度（SpO2）在90%至92%之間（通常為1至2公升/分鐘）。如果無法吸氧，且下山延遲或不切實際，則應給予地塞米松，通常持續24小時（表3）。兒童患者若症狀持續或經治療後加重，則必須下山。
●高山肺水腫 (HAPE) – 與成人一樣，兒童高山肺水腫的治療需要下降海拔和/或吸氧。
●HACE－在極少數疑似兒童HACE的情況下，應立即下撤。補充氧氣、地塞米松和高壓氧治療可以暫時緩解病情，直到完成撤離（表3）。
預防和藥物預防 － 適應環境和緩慢上升是避免高山症的最佳方法。建議前往高海拔地區滑雪、健行或攀岩的旅客在抵達後的頭幾天限制活動。充足的水分攝取也很重要，但應避免過度補水以預防低鈉血症。
為預防急性高山症（及其他高海拔相關症候群），專家建議切勿在一天之內從低海拔地區前往（或在）海拔2750公尺（9000英尺）或更高的地方。此外，已在海拔2500公尺（8200英尺）以上的人，其睡眠海拔不應比前一晚的海拔高出500公尺（1640英尺）以上。對於曾在以往登山過程中出現急性高山症或其他高山症相關問題的人來說，這種方法尤其重要；這些人再次接觸高海拔地區時更容易出現這些疾病。
乙醯唑胺預防 － 尚未有研究探討乙醯唑胺預防性藥物治療在快速上升至海拔3450公尺的兒童的應用。一項前瞻性觀察研究納入了48名快速上升至海拔3450公尺的較大兒童和青少年，結果發現其中18名（38%）出現急性高山症（AMS）症狀，但無一例患者需要接受特殊藥物治療或撤離至較低海拔 [ 40 ]。研究提示，對於大多數未適應高海拔環境的健康較大兒童和青少年，預防性治療可能並非必要。
如果使用乙醯唑胺，治療持續時間取決於上昇路線。對於計劃攀登至固定睡眠海拔高度的人員（例如休閒滑雪者），可在攀登前一天開始服用乙醯唑胺，並持續服用48小時。如果計劃繼續攀登，則可繼續服用乙醯唑胺直至達到最高海拔。乙醯唑胺也可在上升過程中的任何階段間歇性服用，以加速適應海拔或治療輕度急性高山症。在同一海拔高度停藥後，症狀不會復發。雖然經過幾天的適應後，急性高山症的風險會降低，但乙醯唑胺仍可能有助於睡眠。
兒童預防急性高山症（AMS）的乙醯唑胺劑量為每次1.25 mg/kg，每日兩次（單次最大劑量125 mg）（表3）[ 44 ]。對磺胺類抗生素過敏的禁忌症已受到質疑，此類患者服用乙醯唑胺發生過敏性休克的風險似乎不高。另一方面，先前對磺胺類抗生素發生史蒂文斯-約翰遜反應的機制與過敏性休克不同，因此一些臨床醫生選擇不對這類患者使用乙醯唑胺。
高海拔腦水腫 （ HACE）是一種罕見的危及生命的高海拔疾病，理論上可能發生在兒童身上[ 45 ]。在成人中，HACE通常發生在海拔3000至3500公尺（9840至11480英尺）以上的急性高山症（AMS）和/或高海拔肺水腫（HAPE）患者中，具體內容將在其他章節中詳細討論。
高海拔肺水腫 （ HAPE）是一種非心因性肺水腫，可能致命。在美國，低地兒童前往落基山脈高海拔度假勝地後發生HAPE的機率尚不清楚。 HAPE的整體發生率約為萬分之一，其中許多是兒童[ 46 ]。 HAPE可分為三種不同的類型：
●經典型高海拔肺水腫 (cHAPE)—這種類型的肺水腫通常發生在從低海拔上升到高海拔的人群中，或發生在高海拔地區快速上升到更高海拔的人群中。 cHAPE 常見於快速上升到海拔 2500 公尺（8200 英尺）以上睡眠海拔的人群 [ 1 ]，但海拔高度本身不應作為排除該診斷的依據 [ 46 ]。
●重返高海拔肺水腫（rHAPE）－這種疾病常見於從低海拔地區返回家鄉的高海拔居民。
●高海拔居民肺水腫（HARPE）－這種疾病是由高海拔居民在無海拔變化的情況下發生急性呼吸道感染而引發的。
如下列研究所示，居住在高海拔地區然後暫時下降的兒童有高海拔肺水腫的風險。患有急性病毒性上呼吸道感染的兒童前往高海拔地區旅行或居住在高海拔地區，患病風險可能略有增加[ 4,5,18,28,47-49 ]：
●一項回顧性研究分析了科羅拉多州利德維爾市（美國海拔最高的永久居住地，海拔3094米，即10152英尺）32名因高海拔肺水腫（HAPE）住院的患者共39次發作的情況。研究發現，32名患者中有25名年齡在15歲以下，除2名患者外，其餘均為利德維爾市的常住居民[ 18 ]。大多數發作發生在短暫下降到較低海拔之後；其中3名患者的下降時間僅為24小時。研究也發現，HAPE的發生率隨年齡增加而降低，這提示兒童肺血管對海拔的某種未知反應可能是導致兒童HAPE高發生的原因之一。
●在一項針對安第斯山脈 97 名受害者的研究中，也描述了類似的兒童 HAPE 盛行率較高；2 至 12 歲的兒童比年齡較大的患者肺水腫更為嚴重 [ 49 ]。
●一項觀察性研究報告了科羅拉多州利德維爾市七名已從高海拔肺水腫（HAPE）中康復的兒童的心導管檢查結果[ 4 ]。其中三名兒童患有與病毒性上呼吸道感染相關的HAPE，先前並無高山症史。這些患者在缺氧時平均肺動脈壓升高。
●在登山前不久發生的上呼吸道感染（感冒、支氣管炎或中耳炎）似乎也會使居住在低海拔地區的兒童更容易患上高海拔肺水腫（HAPE）；這種現象可能與感染期間發炎介質的釋放有關[ 5 ]。此外，兒童的肺血管反應性比成人更高，發炎會增加毛細血管通透性。這些因素共同導致兒童更容易發生肺水腫。
臨床表現 － 在幼兒中，高海拔肺水腫（HAPE）通常表現為呼吸窘迫在1至2天內逐漸加重，但也可能進展得更為迅速。幼兒和嬰兒可能只表現為蒼白、意識模糊或其他非特異性症狀，例如煩躁不安、哭鬧、食慾下降、玩耍減少、睡眠紊亂，甚至嘔吐[ 6,25,34,35 ]。在嬰兒中，肺動脈壓升高和胎兒分流（無論是否合併HAPE）均可導致嚴重的低氧血症。因此，脈搏血氧飽和度可能低於該海拔的正常值。表4列出了不同海拔和不同暴露條件下動脈血氣分析結果和氧飽和度的平均值和正常值範圍，以幫助解讀結果。 （請參閱 「高海拔肺水腫」章節中的「病理生理學」部分。）
在年齡較大的兒童和青少年中，高海拔肺水腫可能表現為隱性咳嗽、疲乏、與工作量不成比例的呼吸困難、靜止時呼吸困難以及咳出泡沫狀、常呈鐵鏽色的痰液。此時的身體檢查結果包括呼吸急促、紫紺、心搏過速以及肺部聽診可聞及瀰漫性囉音。如有條件，胸部X光片可顯示瀰漫性間質性改變，這是心源性肺水腫的典型表現。 （參見 「非心因性肺水腫」。）
高海拔肺水腫可能在數小時或數天內逐漸出現，但也可能突然發作。它最常發生在高海拔停留兩晚之後。高海拔肺水腫也可能在沒有急性高山症的情況下發生。
單純由高海拔肺水腫引起的體溫升高超過 38.3°C 並不常見；體溫升高應考慮是否有併發感染或其他疾病。對於發燒較高的幼兒，應根據其年齡和免疫接種情況進行評估。然而，呼吸道感染和高海拔肺水腫可能同時存在。
兒童的鑑別診斷包括肺炎、心臟衰竭和其他非心臟性肺水腫。
診斷 — 高海拔肺水腫 (HAPE) 的診斷依賴於典型的臨床表現，包括咳嗽、疲乏、呼吸困難、泡沫痰、肺部聽診可聞及瀰漫性囉音、呼吸窘迫和/或特定海拔高度的低氧血症（表 4），這些症狀通常在高海拔暴露後 1 至 2 天內出現肺炎，且無其他病因（例如肺炎）。在嬰幼兒中，HAPE 可能伴隨其他非特異性急性高山症 (AMS) 症狀，例如煩躁不安、活動減少、食慾減退和嘔吐。如果進行胸部 X 光檢查，則可見瀰漫性間質性改變，符合非心因性肺水腫的表現。
實驗室檢查結果可能包括白血球增多（可能由低壓低氧壓力反應引起）和C反應蛋白升高；這些結果可能提示臨床醫師考慮治療合併感染性疾病[ 50-52 ]。此外，B型鈉尿肽和肌鈣蛋白可能會輕度升高，但通常會隨著病情緩解而迅速恢復正常。
治療 － 對於從低地升到高海拔地區的兒童，HAPE 的治療目標與年齡較大的患者相同：透過增加吸入氧分壓來迅速降低肺動脈 (PA) 壓力和低氧血症 [ 44,53 ]。
選項包括：
●限制體力消耗和寒冷暴露
●透過氧氣罐或製氧機提供補充氧氣
●撤離到較低海拔
●利用高壓氧療法模擬下降
●硝苯地平（≥50 kg）或氨氯地平（<50 kg 或 <17 歲）（表 3）
在這些治療方法中，下降（模擬或實際下降）和/或補充氧氣通常單獨使用最為有效，且似乎優於任何藥物治療。在一些度假區，患有高海拔肺水腫的兒童作為門診病人接受補充氧氣治療，並與家人一起留在原海拔高度，接受密切追蹤。硝苯地平或氨氯地平也被推薦使用（表3）[ 25,46,53 ]。與硝苯地平相比，氨氯地平的優點在於每日一次給藥，且有液體或適當大小的片劑形式，因此更適合幼兒使用。 （請參閱 「高海拔肺水腫」部分的「治療」章節。）
對患有 HAPE 的兒童不當地使用抗生素和利尿劑是無效的，應該避免[ 46 ]。
對於病情嚴重的兒童，尤其是意識障礙的患兒，可能需要透過高流量鼻導管或非侵入性通氣進行吸氧。氣管插管的情況很少見。值得注意的是，重症兒童的病情可能需要一到兩個小時才能明顯好轉，氧氣需求量也會減少。
一小部分患有高海拔肺水腫 (HAPE) 的兒童可能存在潛在的易感疾病。一項研究顯示，17% 的 HAPE 兒童在接受超音波心臟檢查後被診斷出新的心臟結構異常（例如卵圓孔未閉 [PFO] 和房間隔缺損 [ASD]）[ 46 ]。因此，建議進行超音波心臟檢查以評估是否有潛在的肺動脈高壓，並排除已知的危險因素，例如房間隔缺損、導管起源的孤立性肺動脈、主動脈縮窄、室間隔缺損和肺靜脈狹窄 [ 30,46 ]。卵圓孔未閉 (PFO) 可能是危險因素，取決於其大小。
預防 － 與急性高山症一樣，緩慢上升是預防高海拔肺水腫的最佳方法。曾患過高海拔肺水腫的人員應被鼓勵緩慢上升，並做好一旦出現高海拔肺水腫症狀就迅速下降的準備。 （請參閱 「高海拔肺水腫」章節中的「預防」部分。）
對於居住在低海拔地區且無高海拔肺水腫（HAPE）病史的健康兒童，我們建議進行充分的適應性訓練，不建議使用藥物預防HAPE。一些專家基於成人資料和藥物類別效應，建議對易感兒童使用硝苯地平或氨氯地平預防HAPE[ 53 ]。然而，鈣通道阻斷劑在兒童預防HAPE的研究尚不充分。硝苯地平是預防易感成人HAPE的首選藥物，但市售硝苯地平製劑的劑量對兒童而言過大[ 26 ]。在極少數情況下，如果兒童曾發生過HAPE且無法緩慢上升，則使用氨氯地平進行預防可能是合理的選擇。劑量為每日一次口服2.5至5毫克（6至17歲且體重≥25公斤的兒童）或每日一次口服0.1至0.6毫克/公斤/次（最大劑量5毫克/天；1至5歲或體重<25公斤的兒童）。理想情況下，預防性用藥應在登山前24小時開始，並在目的地海拔持續5天（表3）。在高風險情況下，治療可能需要更長時間。
科羅拉多州臨床醫生的經驗表明，乙醯唑胺預防復發性高海拔肺水腫（HAPE）兒童可能有效（表3）。雖然尚未進行正式研究，但已知乙醯唑胺可降低上升至高海拔時的肺動脈壓，並加速適應過程。一些專家建議使用較低的預防劑量（1.25 mg/kg 而非 2.5 mg/kg，每日兩次）。然而，該較低劑量是基於成人研究得出的，在獲得更多兒科特異性數據之前，我們不建議使用該劑量。
其他高海拔相關疾病 － 高海拔視網膜出血和高海拔睡眠週期性呼吸是兒童可能發生的其他高海拔疾病類型。此外，由於兒童體表面積與體重的比值較大，且體內肝醣儲備較少，難以滿足寒冷天氣下增加的能量需求，因此他們更容易發生體溫過低。若照顧者未能妥善保暖，避免兒童暴露於寒冷環境中，幼兒也容易發生凍傷。
高海拔肺動脈高壓 － 嚴重的高海拔肺動脈高壓（HAPH）在健康嬰幼兒中較為罕見。然而，出生少於六週的嬰兒尤其容易發生肺動脈高壓，並可能進展為右心衰竭[ 54 ]。據報道，在出生或抵達海拔3000至5000米（9840至16400英尺）並停留超過一個月的低海拔父母所生的嬰兒中，高達1%的人會患上這種疾病；該病幾乎僅發生於這一群體[ 25 ]。有鑑於此疾病的風險，對於通常生活在低海拔地區或主要在低海拔地區妊娠的六週以下嬰兒，應避免其長時間暴露於高海拔地區[ 32 ]。
6週至1歲的嬰兒若長期暴露於高海拔地區，發生肺動脈高壓伴隨低氧血症、動脈導管未閉（PDA）及卵圓孔未閉（PFO）的風險可能較高[ 13,55 ]。對於將長期停留在高海拔地區的嬰兒，應進行身體檢查和初始脈搏血氧飽和度測量，並在兒童保健就診時定期監測。身體檢查結果提示肺動脈高壓（例如，收縮期噴射性雜音伴隨單音或狹窄分裂的第二心音）或其他結構性心臟病的患者應進行心電圖檢查。如果臨床表現提示結構性心臟病或肺動脈高壓，則還需進行超音波心臟檢查。 （請參閱 「兒童肺動脈高壓：分類、評估和診斷」中的「評估」部分。）
高海拔視網膜出血 － 高海拔視網膜出血（HARH）在海拔4270公尺（14005英尺）以上較為常見，但通常無症狀，因此除非黃斑部受累，否則不易被發現。患者通常主訴視力模糊，眼底檢查可見火焰狀視網膜出血。 與其他高海拔疾病一樣，緩慢上升是預防方法，下降是最佳治療方法。目前尚無藥物可以預防或治療高海拔視網膜出血。任何出現影響視力的出血患者都應下降。視網膜出血會在數週至數月內緩慢消退。
高海拔睡眠週期性呼吸 － 高海拔睡眠週期性呼吸是一種陳-施氏呼吸，幾乎只發生在非快速動眼睡眠期，如果過度換氣階段足夠強烈，可能導致受試者覺醒。兒童可能比成人更不容易出現這個問題。例如，一項針對20名9至12歲兒童及其父親的觀察性研究，比較了他們在海拔3450公尺（11316英尺）和490公尺（1607英尺）睡眠期間的呼吸感應容積描記法、脈搏血氧飽和度和呼氣末二氧化碳測量值。研究發現，與成人相比，兒童的週期性呼吸明顯減少，但過度換氣和夜間血氧飽和度下降的情況與成人相似[ 33 ]。此外，在研究過程中，50%的兒童符合急性高山症（AMS）的診斷標準，而成人的比例為30%。這項發現表明，這些兒童表現出的更穩定的呼吸模式與較低的二氧化碳呼吸暫停閾值有關，但這並不意味著他們對高海拔的耐受性更強。 （請參閱 「高海拔疾病：生理、危險因子和一般預防」一節中的「其他與海拔相關的疾病」。）
給家長/監護人的旅遊建議
健康的嬰兒和兒童 － 六週以上的健康嬰兒和幼兒，包括氣喘控制良好的幼兒，通常都能很好地耐受高海拔旅行，很少會患上嚴重的高海拔病（HAI）。
臨床醫師應避免6週齡以下、出生地或懷孕期間主要在低海拔地區（<1500公尺[4920英尺]）的嬰兒前往高海拔地區旅行，因為他們有突發性嚴重低氧血症、肺動脈高壓和右心衰竭的風險。 （請參閱上文「危險因子」及「高海拔腦水腫」。）
以下措施可降低幼兒發生院內感染的風險或便於管理[ 17 ]：
●逐步上升－一般來說，居住在海拔1500公尺（4920英尺）以下的人應避免突然上升到海拔2750公尺（9000英尺）以上的睡眠地點。最好的方法是在海拔1600米至2200米等中間高度停留一晚（尤其是在前往之前曾引起症狀的海拔高度時）。兩晚則更佳。 （請參閱上文「預防和藥物預防」以及 「高山症：生理、危險因子和一般預防」中關於「逐步或分階段上升」的部分。）
●前兩天避免過度勞累－劇烈的健行、滑雪等活動，應在適應高海拔環境一到兩天後再進行。如果必須進行劇烈運動，例如需要背負重物的健行，攀登速度更需放慢。
●乙醯唑胺預防－大多數專家不會常規地為健康兒童或成人開立乙醯唑胺預防性藥物，尤其是在他們逐漸上升到高海拔地區的情況下[ 1 ]。在無法逐漸上升的情況下（例如，搭乘飛機快速上升到海拔2750公尺[9000英尺]以上的目的地），以及既往在類似海拔和上升速度下反覆出現急性高山症（AMS）的兒童，可能需要進行預防性用藥。然而，兒童既往AMS病史並不能可靠地預測再次發病[ 56 ]。 （請參閱上文「乙醯唑胺預防」。）
●症狀治療－家長或其他照顧者應隨身攜帶布洛芬。適量的布洛芬可以迅速緩解幼兒的煩躁不安或減輕大齡兒童的頭痛。
必要時，也可以開立昂丹司瓊，尤其是在患者睡眠海拔超過 9000 英尺或參加長途跋涉時。
●下降途徑的可用性－如果發生嚴重的高海拔感染，應能迅速採取下降措施。對於難以快速下降的目的地，需要謹慎行事並做好計劃。
●醫療資源－度假社區通常擁有具備醫院感染（HAI）專業知識的醫療保健人員，他們能為家長或其他照顧者提供極佳的醫療資源。如果在這些場所確診醫院感染，通常可以進行有效控制，從而使旅程得以繼續。
臨床醫師應建議照顧者評估偏遠地區的緊急救援或醫療照護能力，以判斷其子女發生醫院感染的風險。
透過適當的教育，大多數家長和照顧者都能辨識出醫院獲得性感染的危險因子、症狀和體徵，即使是語言發展前的兒童也能辨識[ 35 ]。這些知識可以幫助照顧者判斷急性高山症（AMS）的可能性，並依照上述方法進行應對[ 17 ]。 （參見上文「急性高山症」。）
照顧者也應了解，如果患者出現精神狀態改變，例如明顯嗜睡、呼吸困難或共濟失調，應立即就醫。
對於出現輕度 AMS 症狀，可透過下降或藥物治療緩解的兒童，不需要進行特殊評估 [ 17 ]。
通常居住在高海拔地區的兒童，如果出現嚴重的低氧血症或高山肺水腫（HAPE），則需要評估是否有肺動脈高壓或結構性心臟異常[ 4,9 ]。
易感嬰幼兒 － 應建議患有以下疾病的兒童的父母或其他照顧者避免前往高海拔地區旅行[ 13,17 ]（見上文「危險因子」）：
●足月但出生少於六週的嬰兒（早產兒指胎齡不足46週的嬰兒）或有氧療史或肺動脈高壓病史的足月但年齡不超過一歲的嬰兒
●胎齡超過46週且有氧療史、支氣管肺發育不良或肺動脈高壓的早產兒
●先天性心臟病伴隨肺動脈高壓、紫紺或心內分流
●鐮形血球貧血症
●唐氏症合併心臟分流或肺動脈高壓
●活動性呼吸系統疾病，如肺炎、微支氣管炎或囊性纖維化急性惡化
病情穩定的囊性纖維化兒童若能在旅行期間進行脈搏血氧飽和度監測並提供吸氧，則可能可以前往高海拔地區旅行。對於六歲以上的兒童，可以進行第一秒用力呼氣容積（FEV1 ）評估和低氧吸入試驗，這有助於識別哪些兒童在旅行期間需要吸氧[ 26 ]。幾乎所有度假區都有家用氧氣公司，可以接受執照醫生開立的氧氣處方。照顧者應確保兒童在旅行期間嚴格遵守既定的胸部物理治療、祛痰和抗生素治療方案。
患有神經肌肉疾病或限制性肺病（例如嚴重的脊椎側彎）的兒童在旅行前應由兒科肺科醫生進行評估，以確定在高海拔地區是否需要支持措施，例如補充氧氣（持續或夜間）或夜間雙水平正壓通氣[ 26 ]。
病人須知
UpToDate 提供兩種類型的病患教育資料：「基礎知識」和「進階知識」。 「基礎知識」系列文章語言淺顯易懂，閱讀難度相當於小學五六年級水平，解答患者可能對特定疾病提出的四五個關鍵問題。這些文章最適合希望了解疾病概況且偏好簡短易讀資料的患者。 「進階知識」系列文章篇幅更長、內容更深入、更詳細。這些文章的閱讀難度相當於小學十年級至十二年級水平，最適合希望獲得更深入資訊且能夠理解一些醫學術語的患者。
以下是一些與此主題相關的病患教育文章。我們鼓勵您列印或透過電子郵件將這些文章發送給您的患者。 （您也可以透過搜尋「病患資訊」和您感興趣的關鍵字，找到各種主題的病患教育文章。）
●基礎知識主題（參見 「病患教育：高山症（基礎）」）
總結與建議
●海拔高度與高山症風險－高山症的風險取決於個體的易感性、上升速度和到達的海拔高度。海拔超過2500公尺（8200英尺）可能與兒童高山症有關。然而，大多數健康兒童在海拔低於3500公尺（11480英尺）的地方通常不會出現任何嚴重症狀。 （參見上文「兒童高山症」。）
●HAI 的危險因子– 特別容易發生嚴重 HAI 的兒童包括以下幾類
•六週齡以下的嬰兒
•一歲以下有吸氧史或肺動脈高壓病史的嬰兒，包括早產兒
•居住在高海拔地區並經歷短暫下降的兒童
•患有唐氏症、先天性心臟病、囊性纖維化或神經肌肉疾病而影響通氣功能的兒童
年齡較大的兒童和青少年出現急性高山症的症狀與成人相似。最常見的症狀是頭痛，可能伴隨或隨後出現呼吸急促、頭暈、睡眠品質差、食慾不振、疲勞、噁心和嘔吐。
•診斷－急性高山症的診斷依賴於抵達高海拔地區後24小時內出現的典型臨床表現，且排除其他病因（例如中耳炎、肺炎或病毒感染）。對於尚未說話的兒童，急性高山症的診斷屬於排除性診斷。如果在未發現其他病因的情況下，給予補充氧氣（例如，透過鼻導管以2至4公升/分鐘的速度吸氧15至20分鐘）或短暫下降後症狀有所改善，則支持急性高山症的診斷。
•治療－兒童急性高山症的治療依據症狀嚴重程度，遵循與成人相同的原則（表3）。
●高山肺水腫（HAPE）
•臨床表現－雖然在幼兒中罕見，但高海拔肺水腫（HAPE）通常表現為呼吸困難在一到兩天內逐漸加重，但也可能進展得更迅速。在某些幼兒和嬰兒中，早期症狀可能不包括呼吸急促，但氧飽和度始終低於該海拔的正常值（表4）。較大兒童和青少年的HAPE症狀與成人相似：呼吸困難、呼吸急促、肺部囉音、咳出泡沫狀鐵鏽色痰液。 （參見上文「臨床表現」部分。）
•診斷－高海拔肺水腫的診斷依賴典型的臨床表現，這些表現通常在高海拔暴露後一到兩天出現，且排除其他病因（例如肺炎）。如果進行胸部X光檢查，則顯示瀰漫性間質性改變，符合非心源性肺水腫的特徵。 （請參閱上文「診斷」部分。）
•治療－患有高海拔肺水腫的兒童需要立即吸氧、下撤或兩者兼施。在無法吸氧或下撤的緊急情況下，可使用硝苯地平（體重≥50公斤）或氨氯地平（體重<50公斤或年齡<17歲）進行藥物治療，可能有效（表3）。 （參見上文「治療」部分。）
●預防AMS和高海拔肺水腫－對於健康兒童而言，適應環境和緩慢上升是避免AMS和高海拔肺水腫最有效的方法。
•診斷－急性高山症的診斷依賴於抵達高海拔地區後24小時內出現的典型臨床表現，且排除其他病因（例如中耳炎、肺炎或病毒感染）。對於尚未說話的兒童，急性高山症的診斷屬於排除性診斷。如果在未發現其他病因的情況下，給予補充氧氣（例如，透過鼻導管以2至4公升/分鐘的速度吸氧15至20分鐘）或短暫下降後症狀有所改善，則支持急性高山症的診斷。
•治療－兒童急性高山症的治療依據症狀嚴重程度，遵循與成人相同的原則（表3）。
●高山肺水腫（HAPE）
•臨床表現－雖然在幼兒中罕見，但高海拔肺水腫（HAPE）通常表現為呼吸困難在一到兩天內逐漸加重，但也可能進展得更迅速。在某些幼兒和嬰兒中，早期症狀可能不包括呼吸急促，但氧飽和度始終低於該海拔的正常值（表4）。較大兒童和青少年的HAPE症狀與成人相似：呼吸困難、呼吸急促、肺部囉音、咳出泡沫狀鐵鏽色痰液。 （參見上文「臨床表現」部分。）
•診斷－高海拔肺水腫的診斷依賴典型的臨床表現，這些表現通常在高海拔暴露後一到兩天出現，且排除其他病因（例如肺炎）。如果進行胸部X光檢查，則顯示瀰漫性間質性改變，符合非心源性肺水腫的特徵。 （請參閱上文「診斷」部分。）
•治療－患有高海拔肺水腫的兒童需要立即吸氧、下撤或兩者兼施。在無法吸氧或下撤的緊急情況下，可使用硝苯地平（體重≥50公斤）或氨氯地平（體重<50公斤或年齡<17歲）進行藥物治療，可能有效（表3）。 （參見上文「治療」部分。）
●預防AMS和高海拔肺水腫－對於健康兒童而言，適應環境和緩慢上升是避免AMS和高海拔肺水腫最有效的方法。
健康的兒童在攀登至極高海拔地區（超過3500公尺[11480英尺]）時，應緩慢進行，並且只有在出現問題時能夠迅速下降的情況下才應進行。 （請參閱上文「攀登建議」。）
●給家長/監護人的旅行建議－健康兒童通常能很好地適應高山症旅行，很少出現嚴重的高山症。臨床醫師應告知家長或其他監護人，度假社區通常有擅長處理高山症相關問題的醫護人員，如果他們懷疑孩子可能出現高山症，這些醫護人員是很好的資源。 （請參閱上文「給家長/監護人的旅遊建議」。）
INTRODUCTION
This topic will review the unique pediatric aspects of high-altitude illness (HAI).
The different types of HAI, their pathophysiology, and methods for prevention and treatment are discussed separately.
●(See "High-altitude illness: Physiology, risk factors, and general prevention".)
●(See "Acute mountain sickness and high-altitude cerebral edema".)
●(See "High-altitude pulmonary edema".)
●(See "Approach to patients with heart disease who wish to travel by air or to high altitude".)
BACKGROUND
Every year, the beauty and recreational opportunities of the mountains attract millions of visitors from lowland elevations to high-altitude destinations worldwide. Resort towns in the Western United States alone attract over 30 million visitors annually, generally to sleeping elevations of 2000 to 3000 m (6560 to 9840 feet). Many more millions visit cities at these elevations, including several large cities in South America and Asia situated above 3000 m (9840 feet) (table 1) [1]. Most of these destinations can be reached within a day using modern means of transportation. Many of these mountain travelers are children.
Rapid ascents to high altitude place the unacclimatized child at risk for developing high-altitude illness (HAI). Clinicians working in mountainous areas must familiarize themselves with the presentation and management of HAI in children, while all health care workers who advise travelers need to understand the best prevention strategies and treatment options. The clinician advising families with children on wilderness and high-altitude trips should offer an organized pre-trip evaluation that evaluates individual risk factors, provides recommendations for measures to prevent HAI, and determines whether prophylactic medication is appropriate [2]. (See 'Patient risk assessment and mitigation' below and 'Prevention and pharmacologic prophylaxis' below and 'Travel advice for parents/caregivers' below.)
HIGH-ALTITUDE PHYSIOLOGY
Diminished inspired partial pressure of oxygen (PIO2) at altitude is the direct result of lower barometric pressure. As PIO2 decreases, so does the partial pressure of alveolar oxygen (PAO2), arterial PO2 (PaO2), and arterial oxygen saturation (SpO2), resulting in tissue hypoxia. This form of hypoxia is termed hypobaric hypoxia, and it represents the initial cause of high-altitude illness (HAI). The physiology of HAI is discussed in more detail separately. (See "High-altitude illness: Physiology, risk factors, and general prevention", section on 'High altitude physiology'.)
PATIENT RISK ASSESSMENT AND MITIGATION
Risk factors — Risk factors for high-altitude illness (HAI) that are common to children and older patients include rapid rate of ascent, the absolute altitude achieved, the degree of physical exertion, cold weather, and history of prior HAI. (See "High-altitude illness: Physiology, risk factors, and general prevention", section on 'Risk factors'.)
Certain individuals develop high-altitude pulmonary edema (HAPE) upon repeated ascents above the same altitude and may, therefore, have an altitude threshold beyond which they are susceptible to HAPE. Individuals who have experienced multiple HAPE episodes in the past have demonstrated genetic or physiological susceptibility and are therefore at risk for recurrence with ascent to the same altitude and at the same rate. Recurrence in these individuals may be avoided with a slower rate of ascent or with pharmacologic prophylaxis.
Risk factors found more commonly in children include the following:
●Acute illness with upper or lower respiratory tract infection or other infection (eg, otitis media) [3-7]
●Congenital cardiopulmonary disease [8,9] (eg, unilateral absence of pulmonary artery) [10,11]; pulmonary hypertension [3]; cardiac shunts (atrial septal defect, ventricular septal defect, patent foramen ovale)
●Down syndrome, especially with obstructive sleep apnea [3,12]
●Systemic diseases that compromise respiratory function (eg, bronchopulmonary dysplasia [13], cystic fibrosis [14], sickle cell anemia [15], severe scoliosis [16], neuromuscular disease, obstructive sleep apnea)
●Full-term infants less than six weeks of age (premature infants less than 46 weeks post-conceptual age) [13,17]
●Premature and full-term infants who have experienced respiratory distress in the immediate postnatal period; infants up to one year of age with a history of oxygen requirement, bronchopulmonary dysplasia, or pulmonary hypertension [13,17]
●Susceptibility to re-ascent HAPE patient lives at high altitude [above 2500 m, 8200 feet], travels to low altitude for a short time period [eg, several days to weeks], and then returns home rapidly from low altitude) [18,19]
Recommendations for ascent — Healthy children should ascend to high altitudes slowly [20] and only if rapid descent is possible in the event of problems. Children have ascended safely as far as 15,580 to 18,040 feet (4570 to 5500 m). If the child has an acute upper respiratory infection, lower respiratory infection, or otitis media, extra caution should be exercised during rapid ascent above 2500 m (8200 feet) [20]. (See 'Risk factors' above.)
General measures to prevent HAI in children are derived from adult experience and include (see "High-altitude illness: Physiology, risk factors, and general prevention", section on 'Prevention of high-altitude illness'):
●Gradual ascent – Avoid abrupt ascent to sleeping altitudes above 2800 m (9200 feet).
●Acclimatization – Take measures to permit the child to become accustomed to higher altitudes:
•When ascending above 2500 m (8200 feet), do not spend subsequent nights at elevations more than 500 m higher than the previous night.
•Include a rest day (no ascent and no vigorous activity) for every 1000-m (3280-foot) increase in sleeping altitude.
•When possible, spend four to five days at an intermediate altitude (typically 3000 to 4000 m) before proceeding to higher elevations.
Recommendations for children with pre-existing illnesses — Infants and children with certain underlying diseases are at particular risk for significant complications, including exacerbation of their underlying condition or life-threatening high-altitude pulmonary edema (HAPE):
●Sickle cell disease – Patients with sickle cell disease who live at sea level should ascend cautiously if at all, as sickle cell crisis can occur at altitudes as low as 1500 m (4920 feet) [1]; symptoms are common at 2300 m (7544 feet). Patients with sickle cell trait may rarely become symptomatic from splenic sequestration or infarction at altitudes over 2500 m (8200 feet) [21-23].
●Asthma – Patients with asthma may find that their symptoms improve because of a relative lack of allergens at high altitudes. While theoretically bronchospasm induced by cold or exercise may worsen [24], patients with asthma appear to have no higher risk of altitude illness compared with those without asthma [21,25,26].
●Chronic lung disease – Children with chronic lung disease, such as cystic fibrosis or bronchopulmonary dysplasia, are at increased risk of significant hypoxemia and should undergo oxygen saturation monitoring during altitude travel. [27,28]. Again, ascent should be slow and cautious. One author suggests that children who are able to play and run without shortness of breath at home are unlikely to have problems lower than 3650 m (11,972 feet) [21]. Supplemental oxygen may enable other children to travel to altitudes between 2000 to 3000 m (6560 to 9840 feet) [26]. (See 'High-altitude pulmonary edema' below and "High-altitude pulmonary edema", section on 'Epidemiology and risk factors'.)
●Cardiac lesions with increased pulmonary artery blood flow – Infants and children with cardiac lesions involving an increase in pulmonary blood flow or pulmonary hypertension are at increased risk for HAPE. Isolated absence of the right pulmonary artery has been associated with development of HAPE at relatively low altitudes, and these patients should avoid exposure to high altitude [10,29]. Children with other cardiac defects that increase pulmonary flow, such as atrial and ventricular septal defects and patent ductus arteriosus, may be at increased risk for HAPE as well, and may benefit from oxygen saturation monitoring [25,30]. (See 'High-altitude pulmonary edema' below and "High-altitude pulmonary edema", section on 'Epidemiology and risk factors'.)
On the other hand, although an association has been reported between patent foramen ovale (PFO) and HAPE, causality is not established, and PFO is not considered a contraindication to high altitude exposure [31].
●Down syndrome – Children with trisomy 21 have increased pulmonary vascular reactivity and a higher risk of pulmonary hypertension in addition to an increased risk of congenital cardiac defects. They are also more likely to have obstructive sleep apnea and hypoventilation. These factors may be responsible for a higher risk of HAPE, even at relatively low altitudes [3]. Thus, travel to high altitude in children with trisomy 21 should be approached cautiously [25].
●Infants with a history of oxygen therapy or pulmonary hypertension – Infants under one year of age with a history of oxygen requirement or pulmonary hypertension have several unique physiologic limitations that place them at risk for hypoxemia, severe pulmonary hypertension, and, in extreme cases, right heart failure when rapidly exposed to high altitude (3000 to 5000 m [9840 to 16,400 feet]) [13,32]. (See 'Risk factors' above and 'High-altitude cerebral edema' below.)
HIGH-ALTITUDE ILLNESS IN CHILDREN
Acute mountain sickness (AMS) is the most common of the altitude illnesses. The risk of AMS depends upon individual susceptibility, the elevation reached, and the rate of ascent. Thus, while AMS is uncommon below 2000 m (6560 feet), it is quite common (approximately 25 percent incidence in adults and children) at sleeping elevations between 2000 and 3000 m (6560 to 9840 feet), where some cities and the majority of ski resorts in the Western United States are located (table 2 and table 1) [33-36]. In most instances, pediatric high-altitude illness (HAI) can be prevented with appropriate precautions or treated before serious illness, such as high-altitude pulmonary edema (HAPE) or high-altitude cerebral edema (HACE), occurs.
At higher altitudes, small observational studies initially suggested that AMS may occur more frequently in children and adolescents than in adults with ascent in a few hours from sea level to at elevations above 3500 m [33,37,38]. However, larger studies have found either the same incidence as adults or less:
●In one observational study that evaluated the impact of fast ascent among families with 157 children ascending 3450 m in 2.5 hours, AMS in children was lower (30 percent), compared with adolescents (37 percent) and adults (45 percent) [39]. In addition, familial clustering was consistent and explained 25 to 50 percent of variability, the first evidence of hereditary influence for AMS.
●In a separate study of 48 children who underwent the same rapid ascent profile, AMS incidence was 25 percent at 6 hours, 21 percent at 18 hours, and 8 percent at 42 hours; all AMS was mild, and none required descent [40].
●A third study took 118 children ages 6 to 16 in 2.5 hours to 3450 m in the Alps and found only a 6 percent incidence of AMS at 40 hours, confirming the rapid resolution of AMS without treatment [41].
Thus, the overall risk of AMS appears to be the same or less in children compared with adults, and as in adults, slower ascent rates reduce illness.
The epidemiology of AMS in adults is discussed in greater detail separately. (See "Acute mountain sickness and high-altitude cerebral edema", section on 'Epidemiology and Risk factors'.)
Acute mountain sickness — AMS and HACE are generally considered to represent two points along a single spectrum of disease, with the same underlying pathophysiology. Although some aspects of this pathophysiology remain unclear, the concept that AMS/HACE represents a continuum, and that AMS can progress to fatal HACE, fits with clinical experience and is helpful for management. However, especially in young children and infants, recognition of AMS is hampered by the difficulty in recognizing symptoms (eg, headache) in a nonverbal child. Certain pediatric patients (eg, infants under six weeks of age, children with congenital heart disease, cystic fibrosis, or Down syndrome) also have a greater susceptibility for life-threatening disease. (See 'Recommendations for children with pre-existing illnesses' above.)
Clinical manifestations — Signs of AMS in young children are nonspecific and include decreased playfulness, pallor, fussiness, poor sleep, vomiting, and decreased appetite [27,34,35].
In older children and adolescents, signs of HAI are similar to adults; the most common symptom is headache, which may be accompanied or followed by shortness of breath, dizziness, poor sleep, anorexia, fatigue, nausea, and vomiting [36]. The presentation and diagnosis of AMS in adults is discussed in greater detail separately. (See "Acute mountain sickness and high-altitude cerebral edema", section on 'Clinical features'.)
The onset of AMS is usually delayed for 6 to 12 hours following arrival at high altitude but can occur as rapidly as 1 to 2 hours or as late as 24 hours [42,43]. If there is no further ascent, symptoms are often most severe after the first night, generally resolve in one day with rest (eg, no skiing or hiking), and do not recur at the same altitude. AMS may reappear upon ascent to higher altitudes. On occasion, symptoms of AMS may persist for days despite no further ascent. In such cases, descent is required if there is no improvement with standard treatment. (See "Acute mountain sickness and high-altitude cerebral edema", section on 'AMS'.)
Supplemental oxygen may be used to support the clinical diagnosis of AMS. In our experience, providing 2 to 4 L/minute of oxygen by nasal cannula for 15 to 20 minutes prior to other interventions should markedly improve headache and other symptoms, as does a brief excursion to a lower altitude, especially in younger children.
The onset of symptoms more than two days after arrival at a given altitude, absence of headache, dyspnea at rest, and failure to improve rapidly with supplemental oxygen should prompt the clinician to search for an alternative diagnosis. No radiographic or laboratory testing is typically required unless the diagnosis of AMS is unclear. Other etiologies to consider include carbon monoxide poisoning, migraine (including new onset), dehydration, exhaustion, hyponatremia, viral syndrome, bacterial infection (eg, pneumonia or otitis), and occult trauma such as corneal abrasion. In young children, AMS is a diagnosis of exclusion.
AMS alone does not cause an elevation in body temperature, and an appropriate evaluation for fever based upon age and immunization status is warranted in febrile children at altitude. The clinician should pay close attention to the child's signs and response to oxygen, and when in doubt, should err on the side of a longer observation period before attributing symptoms to a condition other than AMS. (See "Fever without a source in children 3 to 36 months of age: Evaluation and management", section on 'Well-appearing patients'.)
Diagnosis — The diagnosis of AMS relies on typical clinical manifestations of vomiting, malaise, pallor, headache, fussiness, and/or difficulty breathing that occurs within 24 hours of arrival at high altitude without evidence of another cause (eg, otitis media, pneumonia, or viral illness). The diagnosis is supported by rapid improvement with supplemental oxygen or descent.
Treatment — The treatment of HAI in children follows the same principles as in adults [44]. All high-altitude illness responds to descent, although it is not always necessary. We find that a descent of 500 m (1600 ft) is sufficient for most children. It is important that group members and the afflicted individual remain alert for any symptoms or signs of worsening disease, particularly at elevations where AMS may rapidly progress to HACE (above 4000 m [13,120 feet]). (See "Acute mountain sickness and high-altitude cerebral edema", section on 'AMS' and "Acute mountain sickness and high-altitude cerebral edema", section on 'HACE'.)
Treatment of HAI is based upon symptom severity:
●Mild AMS – Mild AMS can be treated conservatively with symptomatic care (eg, acetaminophen or ibuprofen for headache, ondansetron for vomiting, rest, and fluid intake). Descent is not generally necessary.
●Moderate to severe AMS – Moderate/severe AMS (ie, AMS not resolving with rest or symptomatic care, or with moderate/severe symptoms) may require descent or supplemental oxygen (if available), and/or specific medication (table 3). Oxygen is most effective when used for a minimum of 2 to 4 hours, although we generally prescribe it for 12 to 24 hours, at a flow rate sufficient to maintain SpO2 at 90 to 92 percent (usually 1 to 2 L/minute). If oxygen is not available, and descent is delayed or impractical, dexamethasone should be administered, usually for 24 hours (table 3). Pediatric patients whose symptoms persist or worsen despite treatment must descend.
●HAPE – As with adults, treatment of HAPE requires descent and/or supplemental oxygen. (See 'High-altitude pulmonary edema' below.)
●HACE – In the exceedingly rare scenario of suspected pediatric HACE, immediate descent is indicated. Supplemental oxygen, dexamethasone, and hyperbaric therapy may temporize illness until evacuation is completed (table 3). (See "Acute mountain sickness and high-altitude cerebral edema", section on 'HACE'.)
Prevention and pharmacologic prophylaxis — Acclimatization and slow ascent are by far the best ways to avoid AMS. Travelers who ascend to high altitudes to ski, hike, or climb should be encouraged to limit their activity for the first few days at altitude. Adequate hydration is also important, although overhydration should be avoided to prevent hyponatremia.
To prevent AMS (and other altitude-related syndromes), experts recommend never traveling to (or sleeping at) 2750 m (9000 ft) or higher in one day from low altitude. In addition, individuals already above 2500 m (8200 feet) should not ascend to a sleeping altitude that is more than 500 m (1640 feet) above the previous night's altitude. This approach is particularly important for individuals who have experienced AMS or other altitude-related problems in previous ascents; such individuals are more likely to suffer from these disorders on subsequent exposure to high altitude. (See "High-altitude illness: Physiology, risk factors, and general prevention", section on 'Preacclimatization'.)
Acetazolamide prophylaxis — Prophylactic pharmacologic therapy with acetazolamide has not been studied in children who undergo rapid ascent. One prospective observational study of 48 older children and adolescents with rapid ascent to 3450 m found that 18 (38 percent) developed symptoms of AMS, but that no patient required specific pharmacologic treatment or evacuation to a lower altitude [40]. This study suggested that prophylactic therapy for AMS may be unnecessary in most healthy older children and adolescents who are not acclimatized.
If acetazolamide is used, the duration of treatment depends upon the ascent profile. Individuals ascending to a fixed sleeping altitude (eg, recreational skiers) may start acetazolamide the day before ascent and continue treatment for 48 hours. If further ascent is planned, acetazolamide can be continued until maximum elevation is attained. Acetazolamide can also be taken episodically to speed acclimatization at any point during altitude gain or to treat mild AMS. Symptoms do not recur when the drug is discontinued while at the same altitude. Although the danger of AMS passes after a few days of acclimatization, acetazolamide may still be useful for sleep. (See "Acute mountain sickness and high-altitude cerebral edema", section on 'Pharmacologic prevention of AMS/HACE' and "Acute mountain sickness and high-altitude cerebral edema", section on 'Preferred: acetazolamide'.)
The pediatric dose of acetazolamide for prevention of AMS is 1.25 mg/kg per dose twice a day (maximum single dose 125 mg) (table 3) [44]. The contraindication due to allergy to antibiotic sulfonamides has been challenged, and the risk of anaphylaxis from acetazolamide in such patients appears unlikely. On the other hand, a history of Stevens-Johnson reaction to an antibiotic sulfonamide is caused by a different mechanism than anaphylaxis, and some clinicians choose not to administer acetazolamide in these patients. (See "Sulfonamide hypersensitivity", section on 'Between sulfonamide antimicrobials and nonantimicrobials'.)
High-altitude cerebral edema — HACE is a rare life-threatening altitude disease that theoretically may occur in children [45]. In adults, HACE generally occurs in individuals with AMS and/or HAPE at elevations over 3000 to 3500 m (9840 to 11,480 feet) and is discussed in more detail separately. (See "Acute mountain sickness and high-altitude cerebral edema" and "High-altitude pulmonary edema", section on 'Epidemiology and risk factors'.)
High-altitude pulmonary edema — HAPE is a form of noncardiogenic pulmonary edema that may be fatal. In the United States, the incidence of HAPE in lowland children visiting high-altitude resorts in the Rocky Mountains is unknown. The overall incidence of HAPE is approximately 1 in 10,000 visitors, and many of these are children [46]. Three distinct forms of HAPE are described:
●Classic HAPE (cHAPE) – This form typically occurs in individuals ascending from low to high altitude, or individuals at high elevation rapidly ascending to higher elevation. cHAPE occurs among individuals who rapidly ascend to sleeping altitudes above 2500 m (8200 feet) [1], although altitude alone should not be used to exclude the diagnosis [46].
●Reentry HAPE (rHAPE) – This form is observed in high-altitude residents returning home from lower elevations.
●High-altitude resident pulmonary edema (HARPE) – This form is triggered in high-altitude residents by acute respiratory infection without altitude change.
As illustrated by the following studies, children who live at high altitudes and then temporarily descend are at risk for HAPE. Children with an acute viral upper respiratory tract infection who travel to or live at high altitude may have a slightly increased risk [4,5,18,28,47-49]:
●In a retrospective review of 39 episodes in 32 patients hospitalized for HAPE in Leadville, Colorado, the highest permanent community in the United States at an altitude of 10,152 feet (3094 m) above sea level, 25 of the 32 patients were under 15 years of age, and all but two victims were permanent residents of Leadville [18]. The majority of episodes followed a brief descent to lower altitudes; in three patients, the descent period was only 24 hours. A decrease in the incidence of HAPE was noted with increasing age, suggesting that an undefined response of the pediatric pulmonary vasculature to altitude may contribute to childhood frequency of HAPE.
●Similar childhood predominance of HAPE also was described in a study of 97 victims in the Andes; children between the ages of 2 and 12 years had more severe pulmonary edema than did older patients [49].
●An observational study reported cardiac catheterization results for seven children who lived in Leadville, Colorado and who had recovered from HAPE [4]. Three children had HAPE in association with a viral upper respiratory tract infection without any prior descent. These patients had a greater mean pulmonary artery pressure in response to hypoxia.
●Upper respiratory infection (colds, bronchitis, or otitis media) in the period immediately preceding ascent also appears to predispose children who live at low altitude to development of HAPE; this phenomenon may be related to the release of inflammatory mediators during infection [5]. Furthermore, children have greater pulmonary vascular reactivity than adults, and inflammation increases capillary permeability. Together, these cause proportionally more pulmonary edema in children.
Clinical manifestations — In young children, HAPE presents as increasing respiratory distress over one to two days, but may develop more precipitously. Young children and infants may manifest only pallor and depressed consciousness or other nonspecific symptoms such as increased fussiness, crying, decreased appetite, decreased playfulness, disrupted sleep, and possibly vomiting [6,25,34,35]. In infants, increased pulmonary artery pressure and fetal shunting, with or without HAPE, can cause severe hypoxemia. Thus, the pulse oximetry may be low relative to normal values at that altitude. The table provides mean values and range of normal values for arterial blood gas results and oxygen saturation at different altitudes and by exposure to assist with interpretation (table 4). (See "High-altitude pulmonary edema", section on 'Pathophysiology'.)
In older children and adolescents, HAPE may present as an insidious cough, fatigue, breathlessness out of proportion to work, breathlessness at rest, and production of frothy, often rusty, sputum. Physical findings at this time include rapid breathing, cyanosis, tachycardia, and diffuse crackles on lung auscultation. When available, a chest radiograph reveals diffuse interstitial changes typical of noncardiogenic pulmonary edema. (See "Noncardiogenic pulmonary edema".)
HAPE may appear over the course of several hours or days, but may also present explosively. It is most common after two nights at a high altitude. It can occur without preceding AMS.
Elevation in body temperature over 38.3°C from HAPE alone is unusual; higher temperatures warrant evaluation for a concurrent infection or another diagnosis. Young children with a higher fever should be assessed based upon age and immunization status. However, respiratory infection and HAPE can coexist. (See "Fever without a source in children 3 to 36 months of age: Evaluation and management", section on 'Well-appearing patients'.)
The differential diagnosis in children includes pneumonia, heart failure, and other forms of non-cardiogenic pulmonary edema. (See "Pathophysiology of left-to-right shunts" and "Isolated ventricular septal defects (VSDs) in infants and children: Anatomy, clinical features, and diagnosis" and "Isolated atrial septal defects (ASDs) in children: Classification, clinical features, and diagnosis" and "Community-acquired pneumonia (CAP) in children: Clinical features and diagnosis", section on 'Clinical presentation'.)
Diagnosis — The diagnosis of HAPE relies on typical clinical manifestations of cough, fatigue, dyspnea, frothy sputum, diffuse crackles on auscultation of the lungs, respiratory distress, and/or hypoxemia for the specific altitude (table 4) that present one to two days after high altitude exposure without evidence of another cause (eg, pneumonia). In infants and young children, HAPE may be accompanied by other nonspecific signs of AMS such as fussiness, decreased activity, decreased appetite, and vomiting. If performed, chest radiographs show diffuse interstitial changes consistent with noncardiogenic pulmonary edema.
Laboratory findings may include leukocytosis (likely from the stress response to hypobaric hypoxia), and elevated C-reactive protein; these may lead clinicians to consider treatment for concomitant infectious processes [50-52]. Additionally, mild increases in B-type natriuretic peptide and troponin may be seen and generally normalize rapidly with resolution of illness.
Treatment — The treatment of HAPE in lowland children who ascend to high altitude targets the same goal as in older patients: the prompt reduction of pulmonary artery (PA) pressure and hypoxemia via increasing the partial pressure of inspired oxygen [44,53].
Options include:
●Limiting physical exertion and cold exposure
●Providing supplemental oxygen via tank or concentrator
●Evacuation to a lower altitude
●Simulating descent using hyperbaric therapy
●Nifedipine (≥50 kg) or amlodipine (<50 kg or <17 years old) (table 3)
Of these treatments, descent (simulated or actual) and/or supplemental oxygen are most often effective alone and appear to be superior to any pharmacologic therapy. In some resort areas, children with HAPE are treated as outpatients with supplemental oxygen and remain at the same altitude with their families with close follow-up. Nifedipine or amlodipine have also been suggested (table 3) [25,46,53]. Compared with nifedipine, amlodipine offers advantages for small children because of once-daily dosing and availability as liquid or appropriately sized tablets. (See "High-altitude pulmonary edema", section on 'Treatment'.)
Inappropriate use of antibiotics and diuretics in children with HAPE is not efficacious and should be discouraged [46].
For severely ill children, especially those with impaired consciousness, supplemental oxygen by high-flow nasal canula or noninvasive ventilation may be necessary. Tracheal intubation is rarely required. Notably, it can take one to two hours for noticeable improvement and reduction in oxygen requirement in severe illness.
A small proportion of children with HAPE may have an underlying predisposing condition. In one study, 17 percent of children with HAPE who underwent echocardiogram were diagnosed with new structural heart findings (eg, patent foramen ovale [PFO] and atrial septal defects [ASDs]) [46]. Thus, an echocardiogram is warranted to evaluate for underlying pulmonary hypertension and to rule out structural abnormalities that are known risk factors, such as an ASD, isolated pulmonary artery of ductal origin, coarctation of the aorta, ventriculoseptal defect, and pulmonary vein stenosis [30,46]. A PFO may be a risk factor, depending on its size.
Prevention — As with AMS, slow ascent is the best method to prevent HAPE. Individuals with previous HAPE should be encouraged to ascend slowly and be prepared to descend quickly if symptoms of HAPE appear. (See "High-altitude pulmonary edema", section on 'Prevention'.)
For healthy children residing at low altitude and without a history of HAPE, we recommend adequate acclimatization and do not use pharmacologic HAPE prophylaxis. Some experts have suggested using nifedipine or amlodipine for prevention of HAPE in susceptible children based on adult data and class effect [53]. However, calcium channel blockers have not been studied specifically in children for HAPE prophylaxis. Nifedipine is the preferred drug for the prevention of HAPE in susceptible adults, but the commonly available nifedipine formulations contain inappropriately large doses for children [26]. In the rare circumstance that a child has had past episodes of HAPE and slow ascent is not possible, prophylaxis with amlodipine would be a reasonable option. The dose is 2.5 to 5 mg orally once daily (child 6 to 17 years old and ≥25 kg) or 0.1 to 0.6 mg/kg/dose orally once daily (maximum 5 mg/day; child 1 to 5 years old or <25 kg). Ideally, prophylaxis is started 24 hours prior to ascent and continued for five days at the destination altitude (table 3). In higher-risk scenarios, treatment may be continued for a longer period. (See "High-altitude pulmonary edema", section on 'Prophylactic medications'.)
Experience among clinicians in Colorado suggests that acetazolamide prophylaxis for children with recurrent re-entry HAPE may be effective (table 3). Although this has not been formally studied, acetazolamide is known to reduce pulmonary artery pressure on ascent to altitude as well as speed acclimatization. Some experts recommend a lower prophylactic dose (1.25 mg/kg instead of 2.5 mg/kg, both twice daily). However, this lower dose is based on adult studies, and we do not suggest its use until further pediatric-specific data are available.
Other altitude-related illness — High-altitude retinal hemorrhage and high-altitude periodic breathing of sleep are other types of altitude illness that may occur in children. In addition, children are more prone to hypothermia because of the larger surface area to mass ratio and the decreased glycogen stores available for increased energy needs in cold weather. Young children are also prone to frostbite if proper attention to appropriate clothing and limitation of cold exposure is not provided by caregivers. (See "Hypothermia in children: Clinical manifestations and diagnosis", section on 'Pediatric considerations' and "Frostbite: Acute care and prevention", section on 'Risk factors'.)
High-altitude pulmonary hypertension — Serious high-altitude pulmonary hypertension (HAPH) is rare in healthy infants and children. However, infants less than six weeks of age are at particular risk for pulmonary hypertension and progression to right heart failure [54]. This entity has been described in up to 1 percent of infants of lowland parents who are born or arrive at high altitude (3000 to 5000 m [9840 to 16,400 feet]) and remain there for more than a month; it occurs almost exclusively in this group [25]. Because of the risk of this disorder, exposure to prolonged high altitude should be avoided in infants younger than six weeks of age who normally live at low altitude or whose gestation primarily occurred at low altitude [32].
Infants between six weeks and one year of age may have a higher incidence of pulmonary hypertension with hypoxia, patent ductus arteriosus (PDA), and PFO with prolonged exposure to high altitudes [13,55]. Those infants who will be remaining indefinitely at altitude warrant physical examination and an initial measurement of pulse oximetry followed by regular monitoring at well child visits. Patients with physical findings suggesting pulmonary hypertension (eg, systolic ejection murmur with a single or narrowly split second heart sound) or other structural heart disease should have an electrocardiogram. An echocardiogram is also necessary if clinical findings suggest structural heart disease or pulmonary hypertension. (See "Pulmonary hypertension in children: Classification, evaluation, and diagnosis", section on 'Evaluation'.)
High-altitude retinal hemorrhage — High-altitude retinal hemorrhage (HARH) is a relatively common finding at altitudes above 4270 m (14,005 feet), but it usually is asymptomatic and thus, unrecognized unless the macula is involved. The usual complaint is blurring of vision and funduscopy shows flame-like retinal hemorrhages. As with all other forms of altitude disease, slow ascent is preventive, and descent is the best treatment. No medications have been found to prevent or treat HARH. Any individual with hemorrhage affecting vision should descend. The retinal hemorrhages resolve slowly over the course of several weeks to months. (See "High-altitude illness: Physiology, risk factors, and general prevention", section on 'Other altitude-related illnesses'.)
High-altitude periodic breathing of sleep — Periodic breathing of sleep at high altitude is a form of Cheyne-Stokes respiration that occurs almost exclusively during non-REM sleep and can awaken subjects if the hyperventilation phase is strong enough. Children may be less disposed to this problem than adults. As an example, an observational study of 20 children between 9 and 12 years of age and their fathers which compared respiratory inductive plethysmography, pulse oximetry, and end-tidal CO2 measurements during sleep at 3450 m (11,316 feet) versus 490 m (1607 feet), children were noted to have markedly less periodic breathing but similar hyperventilation and decrease in nocturnal oxygen saturation compared with adults [33]. Furthermore, 50 percent of children met criteria for AMS versus 30 percent of adults during the course of the study. This finding suggests that the more stable breathing pattern displayed by these children is related to a lower apnea threshold for CO2 and does not render them more tolerant of high altitude. (See "High-altitude illness: Physiology, risk factors, and general prevention", section on 'Other altitude-related illnesses'.)
TRAVEL ADVICE FOR PARENTS/CAREGIVERS
Healthy infants and children — Healthy infants over six weeks of age and young children, including those with well-controlled asthma, typically tolerate travel to altitude well and rarely experience any serious high-altitude illness (HAI).
Clinicians should discourage high altitude travel for infants under six weeks of age who were born at or whose gestations was primarily at low elevation (<1500 m [4920 feet]) because they are at risk for abrupt severe hypoxemia, pulmonary hypertension, and right-sided heart failure. (See 'Risk factors' above and 'High-altitude cerebral edema' above.)
The following measures reduce the risk or enable easy management of HAI in young children [17]:
●Gradual ascent – As a general guideline, individuals who normally reside below 1500 m (4920 feet) elevation must avoid an abrupt ascent to sleeping altitudes above 2750 m (9000 feet). This is best accomplished by spending one night at an intermediate altitude, such as 1600 to 2200 m (particularly when traveling to an elevation that caused symptoms previously). Two nights is even better. (See 'Prevention and pharmacologic prophylaxis' above and "High-altitude illness: Physiology, risk factors, and general prevention", section on 'Gradual or staged ascent'.)
●Avoid overexertion the first two days – Strenuous hiking, skiing, etc, should only follow one to two days of acclimatization. If exertion is unavoidable, such as backpacking that requires carrying a heavy pack, ascent needs to be even slower.
●Acetazolamide prophylaxis – Most experts do not routinely prescribe acetazolamide prophylaxis in otherwise healthy children or adults who are gradually ascending to high altitudes [1]. Prophylaxis may be indicated in situations where gradual ascent is not possible (eg, rapid ascent by airplane to a destination above 2750 m [9000 feet]) and in children who have had repeated episodes of acute mountain sickness (AMS) when previously exposed to a similar altitude and rate of ascent. However, a past history of AMS in children is an unreliable predictor of repeat illness [56]. (See 'Acetazolamide prophylaxis' above.)
●Symptomatic treatment – Parents or other caregivers should travel with ibuprofen. The appropriate dose of ibuprofen can quickly improve fussiness in young children or alleviate headaches in older children.
Ondansetron may also be prescribed for use as necessary, especially if the patient is sleeping over 9000 feet or is participating in a long trek.
●Availability of descent – Descent from altitude should be readily available if serious HAI occurs. Destinations for which rapid descent is difficult require caution and planning.
●Medical resources – Resort communities generally have health care providers with expertise in HAI who are excellent resources for parents or other caregivers. If HAI is diagnosed in these settings, it can usually be managed so that the trip can continue.
Clinicians should counsel caregivers to assess emergency rescue or medical care capabilities in remote settings relative to the risk of HAI in their children.
With proper education, most parents and caregivers can recognize risk factors and symptoms and signs of HAI, even in preverbal children [35]. This knowledge can help caregivers decide when AMS is likely the problem, and how to respond as described above [17]. (See 'Acute mountain sickness' above.)
Caregivers should also know to seek immediate medical attention for altered mental status such as marked drowsiness, respiratory distress, or ataxia. (See 'High-altitude cerebral edema' above and 'High-altitude pulmonary edema' above.)
Children who develop mild AMS that resolves with descent or medication do not require specific evaluation [17].
Children who normally reside at altitude and manifest severe hypoxemia or high-altitude pulmonary edema (HAPE) warrant an evaluation for pulmonary hypertension or structural cardiac abnormality [4,9].
Susceptible infants and children — Parents or other caregivers of children with the following conditions should be advised to avoid travel to high altitude [13,17] (see 'Risk factors' above):
●Full-term infants less than six weeks of age (premature infants less than 46 weeks postconceptual age) or full-term infants up to one year of age with a history of oxygen requirement or pulmonary hypertension
●Premature infants beyond 46 weeks post-conceptual age with a history of oxygen requirement, bronchopulmonary dysplasia, or pulmonary hypertension
●Congenital heart disease with pulmonary hypertension, cyanosis, or intracardiac shunts
●Sickle cell disease
●Down syndrome with cardiac shunts or pulmonary hypertension
●Active respiratory disease such as pneumonia, bronchiolitis, or cystic fibrosis with exacerbation
Children with stable cystic fibrosis may be able to travel to high altitude if pulse oximetry monitoring is performed during travel and supplemental oxygen can be provided. Assessment of FEV1 and hypoxia inhalation testing can be performed in children over six years of age and can help identify those children who warrant supplemental oxygen during the trip [26]. Almost all resort areas have home oxygen companies that honor prescriptions for oxygen written by licensed providers. Caregivers should ensure strict adherence to established chest physiotherapy, mucolytic, and antibiotic regimens during the trip.
Children with neuromuscular disorders or conditions causing restrictive lung disease (eg, severe kyphoscoliosis) should undergo assessment by a pediatric pulmonologist prior to travel to determine the need for supportive measures while at high altitude, such as supplemental oxygen (continuous or nocturnal) or nighttime bilevel positive airway pressure [26].
INFORMATION FOR PATIENTS
UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topic (see "Patient education: High-altitude illness (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Altitude and risk for high-altitude illness (HAI) – The risk of HAI depends upon individual susceptibility, the rate of ascent, and the elevation reached. Ascent above 2500 m (8200 feet) may be associated with HAI in children. However, most healthy children do well without any serious effects at altitudes less than 3500 m (11,480 feet). (See 'High-altitude illness in children' above.)
●Risk factors for HAI – Children at particular risk for serious HAI include the following (see 'Risk factors' above and 'High-altitude cerebral edema' above and 'High-altitude pulmonary hypertension' above):
•Infants under six weeks of age
•Infants up to one year of age with a history of oxygen requirement or pulmonary hypertension, including premature infants
•Children who live at very high altitude and undergo a temporary descent
•Children with Down syndrome, congenital heart disease, cystic fibrosis or neuromuscular problems compromising ventilation
●Acute mountain sickness (AMS)
•Clinical manifestations – Clinical manifestations of AMS are nonspecific in young children and infants and include decreased playfulness, pallor, fussiness, poor sleep, vomiting, and decreased appetite (table 5). A high index of suspicion is required for detection. (See 'Clinical manifestations' above.)
Symptoms of AMS in older children and adolescents are similar to those seen in adults. The most common symptom is headache, which may be accompanied or followed by shortness of breath, dizziness, poor sleep, anorexia, fatigue, nausea, and vomiting. (See "Acute mountain sickness and high-altitude cerebral edema", section on 'Clinical features'.)
•Diagnosis – The diagnosis of AMS relies on typical clinical manifestations that occur within 24 hours of arrival at high altitude without evidence of another cause (eg, otitis media, pneumonia, or viral illness). AMS is a diagnosis of exclusion in preverbal children. Improvement of symptoms after administration of supplemental oxygen (eg, 2 to 4 L/minute by nasal cannula for 15 to 20 minutes) or a brief descent supports the diagnosis of AMS if no other cause is found. (See 'Diagnosis' above.)
•Treatment – Children with AMS are treated based upon symptom severity following the same principles as in adults (table 3). (See 'Treatment' above.)
●High-altitude pulmonary edema (HAPE)
•Clinical manifestations – Although rare in young children, HAPE presents as increasing respiratory distress over one to two days, but may develop more precipitously. In some young children and infants, primary signs may not include tachypnea, but oxygen saturation will always be low relative to normal values at that altitude (table 4). Symptoms of HAPE in older children and adolescents are similar to those in adults: dyspnea, tachypnea, rales, and cough productive of frothy, rusty sputum. (See 'Clinical manifestations' above.)
•Diagnosis – The diagnosis of HAPE relies on typical clinical manifestations that present one to two days after high-altitude exposure without evidence of another cause (eg, pneumonia). If performed, chest radiographs show diffuse interstitial changes consistent with noncardiogenic pulmonary edema. (See 'Diagnosis' above.)
•Treatment – Children with HAPE warrant immediate supplemental oxygen, descent or both. In emergency settings without the option of oxygen or descent, pharmacotherapy with nifedipine (≥50 kg) or amlodipine (<50 kg or <17 years old) may be effective (table 3). (See 'Treatment' above.)
●Prevention of AMS and HAPE – Acclimatization and slow ascent are the most effective ways to avoid AMS and HAPE in otherwise healthy children. (See 'Prevention and pharmacologic prophylaxis' above and 'Prevention' above.)
Healthy children should ascend to very high altitudes (over 3500 m [11,480 feet]) slowly and only if rapid descent is possible in the event of problems. (See 'Recommendations for ascent' above.)
●Travel advice for parents/caregivers – Healthy children generally tolerate travel to altitude well and rarely experience any serious HAI. The clinician should advise parents or other caregivers that resort communities generally have health care providers with expertise in altitude-related problems who are excellent resources if they feel their child might be experiencing HAI
