高海拔肺水腫(HAPE)臨床表現. 底下資料來自 uptodate 網站
1. 初始症狀沒有特異性, 就像感冒症狀, 容易被忽略
2. 罹患HAPE的人, 大約一半會同時罹患AMS急性高山病
3. 經過給氧治療可快速改善(通常10-15分鐘內)
其他疾病,例如心衰竭,腎衰竭
4. 同一海拔待七天後, 如果沒有發生HAPE腫, 之後不太可能發生HAPE
下面是google翻譯的
成人的表現
症狀和體徵 — HAPE 通常開始於輕微的干咳和用力時氣短，通常是在上坡行走時 [ 9,13 ]。這種非特異性症狀很容易被誤認為是良性上呼吸道感染或歸因於高海拔或疲憊時的正常呼吸困難。最初的症狀通常在到達新高度後兩到四天出現。偶爾，HAPE 會急劇發展。這種情況更常發生在夜間或劇烈運動後。在同一海拔高度一周後，HAPE 幾乎不再出現。
隨著 HAPE 的進展，呼吸困難在休息時變得明顯，並且在任何嘗試用力時都變得嚴重。即使在水平面上行走也變得費力。HAPE 的主要臨床特徵是早期從勞力性呼吸困難進展為靜息時呼吸困難。在大約 50% 的病例中，HAPE 伴有急性高山病 [ 10 ]。(參見 “急性高山病與高原腦水腫” )
隨著症狀的進展，咳嗽可能會咳出粉紅色、泡沫狀的痰，並可能產生鮮血。嚴重受限的運動耐力會變得虛弱，嚴重的低氧血症可能危及生命，而沒有迅速下降或補充氧氣。嚴重的低氧血症可能會導致嗜睡或伴隨高原腦水腫 (HACE)。
體格檢查常見心動過速、呼吸急促和低燒（最高 38°C）。最初，吸氣濕羅音可能在右中葉更為突出，但隨著 HAPE 的進展而變得雙側和彌散。右中葉的聽診最好在中外側胸壁進行。頸動脈體功能遲鈍的人，無論是遺傳性的還是獲得性的（例如，頸動脈內膜切除術、頸部放療），可能都沒有呼吸道症狀，而是出現嗜睡、意識模糊和其他中樞神經系統症狀和發現，這些症狀和發現可能更常與 HACE 相關。
氧飽和度 — 脈搏血氧飽和度顯示飽和度值 (SpO 2) 至少比預期高度低 10 點，絕對值可能低至 40% 到 50%。通常情況下，考慮到低氧血症的嚴重程度，患者的表現比預期的要好，並且氧飽和度會隨著吸氧而迅速改善（通常在 10 到 15 分鐘內）。 在 X 光片上看到的嚴重浸潤性肺過程中，SpO 2 的這種快速校正和補充氧氣的臨床狀態實際上是 HAPE 的特徵性特徵，因為其他肺部過程（例如，肺炎，急性失代償性心力衰竭）不會發生這種情況能夠引起如此嚴重的低氧血症並伴有瀰漫性爆裂音或乾囉音。
因此，脈搏血氧儀通常是區分 HAPE 與其他疾病的有用工具。然而，預期的 SpO 2 值隨許多因素而變化，包括海拔高度、適應程度和速度、患者的缺氧通氣驅動和測量方法（例如，脈搏血氧儀之間的差異）；因此應該仔細解釋。SpO 2 在高海拔地區的第一天最低，並在四天內上升到接近最大值，通常比第一天高 3 到 5 個點。儘管正常個體在任何給定海拔高度的預期值都可能有很大差異，但比較 SpO 2 與同一旅行團中一起到達高海拔地區的其他人進行測量有助於建立相對“正常”範圍。下圖提供了 SpO 2 和其他參數在一定海拔範圍內的近似平均值（圖 1 和 表 3）。
在兒童中的表現 — 在兒童中，HAPE 通常表現為在一到兩天內呼吸窘迫加重，但也可能發展得更突然。年幼的兒童可能僅表現出蒼白或紫紺和意識低落，但大多數會出現呼吸急促、低氧血症和濕囉音 [ 14 ]。在嬰兒中，肺動脈壓升高和胎兒分流，沒有 HAPE，可導致嚴重的低氧血症。(參見 上文‘病理生理學’ 和 “高原病：獨特的兒科注意事項” )
單獨的 HAPE 不會 導致 體溫升高超過 38.3°C（101°F），並且應該評估體溫較高的幼兒是否有其他發熱原因。呼吸道感染和HAPE可並存。(參見 “3-36 月齡兒童不明原因發熱的評估和處理” )
兒童的鑑別診斷包括肺炎、未檢測到的心內分流和（嬰兒）因高原肺動脈高壓而開放胎兒分流。一些作者建議對發生 HAPE 的兒童進行結構性心臟問題評估 [ 14,15 ]。（參見 “左向右分流的病理生理學” 和 “嬰兒和兒童孤立性室間隔缺損 (VSDs)：解剖學、臨床特徵和診斷” 和 “兒童孤立性房間隔缺損 (ASDs)：分類、臨床特徵”和診斷” 和 “兒童社區獲得性肺炎：臨床特徵和診斷”，關於‘臨床表現’一節。）
CLINICAL PRESENTATION
Presentation in adults
Symptoms and signs — HAPE generally begins with a subtle, nonproductive cough, and shortness of breath with exertion, often when walking uphill [9,13]. Such nonspecific symptoms are easily mistaken for a benign upper respiratory tract infection or attributed to normal breathlessness at high altitude or exhaustion. Initial symptoms typically appear two to four days after arrival at a new altitude. Occasionally, HAPE develops precipitously. This occurs more often at night or after severe exertion. HAPE almost never develops after a week at the same altitude.
As HAPE progresses, dyspnea becomes noticeable at rest and severe with any attempt at exertion. Even walking on a level surface becomes an effort. A cardinal clinical feature of HAPE is the early progression from dyspnea with exertion to dyspnea at rest. In about 50 percent of cases, HAPE is accompanied by acute mountain sickness [10]. (See "Acute mountain sickness and high-altitude cerebral edema".)
As symptoms progress, the cough can become productive of pink, frothy sputum and may produce frank blood. Severely restricted exercise tolerance becomes debilitating, and severe hypoxemia may become life threatening without prompt descent or supplemental oxygen. Severe hypoxemia may cause drowsiness or concomitant high-altitude cerebral edema (HACE).
On physical examination, tachycardia, tachypnea, and low-grade fever (up to 38°C) are common. Inspiratory crackles may be more prominent in the right middle lobe initially but become bilateral and diffuse as HAPE progresses. Auscultation of the right middle lobe is best performed at the mid-lateral chest wall. Persons with blunted carotid body function, genetic or acquired (eg, carotid endarterectomy, neck radiation), may present without respiratory symptoms and instead with drowsiness, confusion, and other central nervous system symptoms and findings that might more commonly be associated with HACE.
Oxygen saturation — Pulse oximetry reveals saturation values (SpO2) at least 10 points lower than expected for the altitude, and absolute values may be as low as 40 to 50 percent. Typically, the patient appears better than expected given the severity of hypoxemia, and the oxygen saturation improves promptly (usually within 10 to 15 minutes) in response to supplemental oxygen. This rapid correction of the SpO2 and clinical status with supplemental oxygen in the setting of a severe infiltrative lung process seen on radiograph are virtually pathognomonic for HAPE, as this does not occur with other pulmonary processes (eg, pneumonia, acute decompensated heart failure) capable of causing such severe hypoxemia and associated with diffuse crackles or rhonchi.
Thus, pulse oximetry is often a useful tool for distinguishing HAPE from other conditions. However, expected SpO2 values vary with a number of factors, including the altitude, degree and rate of acclimatization, patient's hypoxic ventilatory drive, and method of measurement (eg, variation among pulse oximeters); and therefore should be interpreted carefully. SpO2 is lowest on the first day at high altitude and rises over four days to a near-maximum value, usually 3 to 5 points higher than day one. Although expected values can vary widely in normal individuals at any given altitude, comparing SpO2 measurements with others in the same travel group who arrived at high altitude together can help to establish a relative "normal" range. The following figures provide approximate average values for SpO2 and other parameters at a range of altitudes (figure 1 and table 3).
Presentation in children — In children, HAPE typically presents as increasing respiratory distress over one to two days but may develop more precipitously. Young children may manifest only pallor or cyanosis and depressed consciousness, though most will have tachypnea, hypoxemia, and crackles [14]. In infants, increased pulmonary artery pressure and fetal shunting, without HAPE, can cause severe hypoxemia. (See 'Pathophysiology' above and "High-altitude disease: Unique pediatric considerations".)
HAPE alone does not cause an elevation in body temperature over 38.3°C (101°F), and young children with a higher temperature should be assessed for other causes of fever. Respiratory infection and HAPE can coexist. (See "Fever without a source in children 3 to 36 months of age: Evaluation and management".)
The differential diagnosis in children includes pneumonia, undetected intracardiac shunts, and (in infants) opening of fetal shunts in response to high-altitude pulmonary hypertension. Some authors suggest that children who develop HAPE should be evaluated for structural heart problems [14,15]. (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 in children: Clinical features and diagnosis", section on 'Clinical presentation'.)
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