之前寫在另一篇筆記. 不過該篇內容越來越龐大. 所以將危險因子的段落摘出來重寫一篇
參考資料 uptodate High altitude pulmonary edemaHAPE=high altitude pulmonary edmea 高海拔肺水腫
HACE=high altitude cerebral edmea 高海拔腦水腫
高海拔肺水腫 HAPE 可簡單分成兩類
1. 一般遊客或登山客, 平常住在低海拔地區, 當進入高海拔地區出現肺水腫症狀
2. 住在高海拔地區的民眾, 去了低海拔地區一段時間, 回到高海拔住所時出現肺水腫症狀 (re-entry 再進入)
其實還有另一類, 是住在高海拔地區的小孩, 在原海拔發生肺水腫合併呼吸道感染
(沒有海拔變化卻出現肺水腫)
(在低海拔, 小孩感冒發生肺水腫屬於比較罕見的狀況)
HAPE通常發生在海拔 2500 公尺以上, 但三千公尺以下不常見.
以四天時間上升到海拔 4500 公尺, HAPE發生率 0.2%
以一兩天時間上升到海拔 4500 公尺, HAPE 發生率 6%
海拔 5500 公尺. HAPE 發生率 2-15%
罹患HAPE的人, 有很高比例也會發生AMS, 罹患HAPE之後會造成嚴重缺氧, 因而同時罹患 HACE.
HAPE危險因子包括
1. 個體對低氧低壓的感受性
2. 到達的海拔高度
3. 上升到高海拔地區速率
4. 在高海拔停留時間
5. 男性較女性容易發生
6. 寒冷 (患者應注意保溫)
7. 有上呼吸道感染(感冒)
8. 激烈運動 (患者應限制不要做激烈活動)
9. 某些狀況或疾病會增加肺部血流量, 造成肺高壓, 增加肺部血管反應, 也容易誘發HAPE (甚至發生在海拔2500公尺以下). 這包括所有會造成肺動脈高壓的狀況, 先天性單側肺動脈缺失, 心臟內分流 intracardiac shunts, 例如心房中膈缺損或心室中膈缺損.
休息與保溫, 被放在HAPE的非藥物治療裡面
高強度活動與冷刺激都會讓肺動脈壓力上升. 可能造成HAPE急性發作
因此. 治療HAPE患者, 限制患者運動量, 避免暴露在寒冷, 是治療HAPE的基本原則
因此, 罹患HAPE的人, 下降過程建議不要背負東西(輕裝或無裝)
臥床休息有沒有幫助, 目前不知道. 但曾有一篇秘魯研究報告說, 在海拔 3750 公尺, 36個輕度至中度 re-endry HAPE 患者, 單純臥床休息就幾乎快痊癒, 而使用氧氣加上臥床靜養, 效果更好. 之後的研究通常是臥床 + 給氧一起做.
在科羅拉多州的滑雪勝地, 通常不會要求在客房內使用氧氣治療的HAPE患者需嚴格臥床休息.
*心臟內分流 intracardiac shunts: 正常心臟內的血流方向是右心房>>右心室>>肺動脈>>肺部微血管>>肺靜脈>>左心房>>左心室>>主動脈>>全身, 當心臟血流以非正常流向流動, 就稱為 shunt 分流. 例如左心室的血經過心室中膈缺損流入右心室. 左心房的血經過心房中膈缺損流入右心房.
開放性卵圓孔 PFO缺氧狀態導致肺血管收縮, 肺血管阻力上升時, 血流會經由 PFO 從右心房流向左心房, 右心房的血是全身含氧量最低的, 混合右心房與左心房的血, 流入左心室, 經主動脈輸送到全身, 會加重血中缺氧, 容易罹患 HAPE 的人, 發現 PFO 機率會增加四倍, 較大的 PFO 會讓動脈缺氧情況更嚴重, 成直接正相關, 發生 HAPE 的機率也會增加, 但 PFO 並不會造成肺動脈壓力大幅上升, 是否PFO會造成 HAPE, 或PFO僅僅是血管反應增加及容易罹患 HAPE 的指標, 目前仍未明. 對於容易罹患HAPE的人, 並不需要為了避免HAPE而去關閉 PFO.
EPIDEMIOLOGY AND RISK FACTORS
HAPE is divided into two types:
●Classic HAPE, involving acute ascent of those normally residing at low altitude
●Re-entry HAPE, involving re-ascent of those normally residing at high altitude after a stay at low altitude
Another category has been suggested for children living at high altitude who develop pulmonary edema with respiratory infection but without a change in altitude [7].
HAPE generally occurs above 2500 meters (8000 feet) and is uncommon below 3000 meters (10,000 feet) (table 1 and table 2) [8,9]. The risk depends upon individual susceptibility, altitude attained, rate of ascent, and time spent at high altitude. In those without a history of HAPE, the incidence is 0.2 percent with ascent to 4500 meters (14,800 feet) over four days but 6 percent when ascent occurs over one to two days. In those with a history of HAPE, recurrence is 60 percent with an ascent to 4500 meters over two days. At 5500 meters (18,000 feet), the incidence ranges between 2 and 15 percent, again depending upon rate of ascent.
Symptoms of acute mountain sickness develop in a high percentage of those with HAPE [10,11]. HAPE and high-altitude cerebral edema (HACE) may also occur concomitantly due to the severe hypoxemia of HAPE.
Factors associated with an increased incidence of HAPE include male sex, cold ambient temperatures, pre-existing respiratory infection, and vigorous exertion [10]. Pre-existing conditions or anatomic abnormalities that lead to increased pulmonary blood flow, pulmonary hypertension, or increased pulmonary vascular reactivity may predispose to HAPE, even at altitudes below 2500 meters. These include pulmonary hypertension of any etiology, congenital absence of one pulmonary artery, and intracardiac shunts, such as atrial septal defects and ventricular septal defects.
A patent foramen ovale (PFO), in the setting of rising pulmonary vascular resistance during hypoxic pulmonary vasoconstriction, may reverse the direction of blood flow, shunting blood from right to left and further exacerbating hypoxemia. PFO is four times more common among HAPE-susceptible individuals. Larger PFOs correlate directly with increased arterial hypoxemia and a trend toward an increased risk of developing HAPE. However, PFO does not cause a greater rise in pulmonary artery pressure [12]. Whether PFO contributes to HAPE or is merely a marker of increased vascular reactivity and susceptibility remains unknown. There is currently no indication for closing PFO in susceptible persons in hopes of preventing HAPE.
TREATMENT
General approach to treatment —
Nonpharmacologic interventions
Oxygen —
Rest and warmth — Strenuous physical exertion and cold stress both elevate pulmonary artery pressure and can exacerbate HAPE. Thus, limiting exertion and avoiding exposure to cold are fundamental aspects of treatment. A patient with HAPE, for example, should not carry a pack while descending. The role of bedrest is unclear. A study with 36 patients with mild to moderate re-entry HAPE at 3750 meters in Peru showed that while bedrest alone resulted in complete recovery, bedrest with oxygen was more effective [35]. Most subsequent studies have used the combination of bedrest and oxygen [32,33,36]. In the Colorado ski resorts, we generally do not recommend strict bedrest during oxygen therapy in the patient's domicile.
Descent —
Hyperbaric therapy —
Positive airway pressure and other therapies
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