Pulmonary edema

Japanese: 肺水腫

(1) Pulmonary edema
Definition Pulmonary edema is defined as abnormal accumulation of fluid outside the pulmonary vasculature.
Mechanism of Pathogenesis Fluid balance in the pulmonary microvasculature is determined by Starling's equation: Q _f = K _f (ΔP−σΔπ)
Here, Q _f is the amount of body fluid that flows out of the blood vessels, K _f is the filtration coefficient, ΔP is the difference in hydrostatic pressure inside and outside the microvessels, σ is the repulsion coefficient for protein, and Δπ is the difference in colloid osmotic pressure inside and outside the microvessels. The mechanisms for draining edema fluid include the lymphatic system, pulmonary and bronchial circulation, thoracic cavity, mediastinum, and bronchial system. If the amount of edema fluid increases and it cannot be drained in time, it will result in pulmonary edema.
Pulmonary edema initially progresses to interstitial and then alveolar edema.
Based on the mechanism of onset, pulmonary edema is classified into 1) hydrostatic pulmonary edema, 2) increased permeability pulmonary edema, and 3) mixed pulmonary edema. An increase in ΔP and a decrease in Δπ cause hydrostatic pulmonary edema, while a decrease in σ and an increase in _Kf cause increased permeability pulmonary edema.
As a disease, it is classified as shown in Table 7-10-3.
Pathological cardiogenic pulmonary edema is the most common type of hydrostatic pulmonary edema. The lungs increase in volume and weight, and a foamy pink liquid leaks from the cut surfaces and bronchi. Histologically, interstitial edema around blood vessels and bronchi and intraalveolar edema are seen.
In pulmonary congestion, phagocytes containing hemosiderin granules, i.e., heart failure cells, are found in the alveoli, and the walls of the pulmonary arterioles and capillaries are thickened with fibrin deposits and increased connective tissue, and the lumen is filled with red blood cells. Furthermore, in chronic cases, pulmonary hemosiderosis may occur.
In acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) that causes hyperpermeability pulmonary edema, histological findings include pulmonary edema, hemorrhage, hyaline membrane formation, and cellular infiltration mainly consisting of neutrophils, which are signs of diffuse alveolar damage (DAD).
Pathophysiological pulmonary edema can be broadly divided into cardiogenic and non-cardiogenic pulmonary edema.
In cardiogenic pulmonary edema, the basic structure of the lungs is maintained, and hypoxemia is easily improved by oxygen inhalation. Orthopnea is used to relieve pulmonary congestion. On the other hand, the pathophysiology of non-cardiogenic pulmonary edema varies depending on the underlying disease, and diagnosis and treatment are often difficult. Acute respiratory distress syndrome (ARDS) and other conditions are often accompanied by intrapulmonary shunt conditions, and hypoxemia is difficult to improve even with oxygen administration.
Clinical symptoms Cardiogenic pulmonary edema is characterized by wheezing, dyspnea, especially paroxysmal nocturnal dyspnea and orthopnea, coughing, and production of frothy pink sputum. Physical examination reveals labored breathing, tachypnea, tachycardia, and distended jugular veins. The skin is pale, cool, and clammy, with cyanosis, and the patient may go into shock. On auscultation, coarse crackles are heard in the lungs.
ALI/ARDS is an increased permeability type pulmonary edema that accounts for the majority of noncardiogenic pulmonary edema. It often presents with unique clinical manifestations depending on the cause. During the course of the underlying diseases shown in Table 7-10-3, patients present with treatment-resistant acute respiratory failure, and chest imaging reveals infiltrative shadows in both lungs.
Neurogenic pulmonary edema is pulmonary edema associated with acute and severe central nervous system disorders such as subarachnoid hemorrhage and seizures. The main mechanism of onset is thought to be the involvement of the sympathetic nervous system due to increased ventricular pressure.
Reexpansion pulmonary edema occurs when a lung that has been collapsed due to pneumothorax or pleural effusion is suddenly re-expanded. It is more likely to be seen when the degree of collapse is severe and the duration of collapse is long.
High-altitude pulmonary edema occurs when healthy individuals with no cardiac or pulmonary abnormalities suddenly reach altitudes of 2,500 m or higher. It generally appears within 2 to 3 days after reaching high altitude. It may be accompanied by retinal hemorrhage and cerebral edema. It quickly improves with transportation to a lower altitude.
Test Results Cardiogenic pulmonary edema appears as air space consolidation on chest X-rays and is often accompanied by cardiomegaly. Blood BNP concentrations often rise as heart failure worsens. Diagnosis of noncardiogenic pulmonary edema is sometimes difficult on chest X-rays, but chest CT shows ground glass opacity but is not accompanied by cardiomegaly (Figure 7-10-5). In all types of pulmonary edema, arterial blood gas analysis shows hypoxemia and respiratory alkalosis.
Mechanism of onset and differential diagnosis: The following methods can be used to clinically differentiate between hydrostatic and hyperpermeability types.
1) Chest imaging diagnosis:
In cardiogenic pulmonary edema, the cardiac shadow and pulmonary vascular shadow are enlarged. The contours of the blood vessels and bronchi become thickened and unclear due to edema (cuffing sign). In severe pulmonary edema, the edema shadow may appear butterfly or bat's wing-like from both hilum to the center of the lung field. If central venous pressure increases, the shadow of the superior vena cava widens and the azygos vein also expands. Pleural effusion, particularly on the right side, is observed. Localized pleural effusion resembles a tumor and improves with treatment, so it is called a vanishing tumor (Figure 7-10-6). Kerley B lines due to edema of the interlobular septum can also be seen.
On the other hand, in hyperpermeability pulmonary edema, unlike cardiogenic pulmonary edema, there is no cardiac enlargement, and no enlargement of the pulmonary vascular shadow or superior vena cava is observed.
2) Measurement of pulmonary artery wedge pressure (P _wp ) using a Swan-Ganz catheter:
It is useful for distinguishing between cardiogenic and noncardiogenic pulmonary edema. In the Forrester classification, a P _wp of ≥ 18 mmHg is defined as left heart failure, and cardiogenic pulmonary edema is diagnosed.
3) Analysis of pulmonary edema fluid:
If a large amount of pulmonary edema fluid is collected, it is possible to differentiate between these diseases based on their cellular components and biochemical analysis. For example, the protein concentration ratio of pulmonary edema fluid to blood is 0.5 or less in hydrostatic pulmonary edema and 0.7 or more in hyperosmotic pulmonary edema.
Diagnosis: Diagnosis of typical pulmonary edema is not difficult based on the clinical features. It is also easy to diagnose the underlying disease if there is preceding chronic heart disease, but if there is no heart disease, it may be necessary to differentiate between severe pneumonia, pulmonary embolism, etc.
Treatment is primarily focused on improving hypoxemia, treating pulmonary edema, and treating the underlying disease. The patient should rest in a semi-upright position and be encouraged to expectorate sputum. Oxygen inhalation should be administered to maintain _PaO2 _{at 60} torr ( _SpO2 _at 90%) or above. The basic approach to treating pulmonary edema is to lower the intravascular pressure of the pulmonary arteries, even in cases of hyperpermeability. For cardiogenic pulmonary edema, treatment for heart failure, including the administration of diuretics, is the mainstay. Treatment for ALI/ARDS, which is permeability pulmonary edema, differs depending on the underlying disease that caused it. [Kimura Hiroshi]
■ References
Crandall ED, Staub NC, et al: Recent developments in pulmonary edema. Ann Intern Med, 99: 808-822, 1983.
Fraser RS, Colman N, et al: Synopsis of Disease of the Chest, 3rd ed, Elsevier, Philadelphia, 2005.

Table 7-10-3
Classification of pulmonary edema ">

Table 7-10-3

Source : Internal Medicine, 10th Edition About Internal Medicine, 10th Edition Information

Japanese:

（1）肺水腫（pulmonary edema）
定義
　肺水腫は肺血管外での異常な液体貯留と定義される．
発症機序
　肺微小血管での水分平衡はStarlingの式により規定される．　　　　　　　Q_f＝K_f（ΔP−σΔπ）
　ここで，Q_f：血管外へ流出する体液量，K_f：濾過係数，ΔP：微小血管内外の静水圧差　σ：蛋白質に対する反撥係数，Δπ：微小血管内外の膠質浸透圧差．　水腫液の排出機構として，リンパ系，肺・気管支循環系，胸腔，縦隔，気管支系がある．　水腫液が増加し排出が間に合わないと肺水腫となる．
初期には間質性，次いで肺胞性肺水腫へと進展する．
分類
　発症機序から，①静水圧性（hydrostatic）肺水腫②透過性亢進型（increased permeability）肺水腫③混合型肺水腫に分類される．　ΔPの上昇およびΔπの低下が静水圧性肺水腫，σの低下，K_fの増加が透過性亢進型の肺水腫を惹起する．
　疾患としては，表7-10-3のように分類される．
病理
　心原性肺水腫は静水圧性肺水腫のなかで最も頻度が高く，肺は容積と重量を増し割面や気管支からは泡沫ピンク色の液体が流出する．組織学的には血管・気管支周囲の間質性浮腫や肺胞内浮腫がみられる．
　肺うっ血（pulmonary congestion）では，肺胞にヘモジデリン顆粒を含む食細胞，すなわち心不全細胞（heart failure cell）がみられ，肺小動脈や肺毛細血管壁は肥厚しフィブリン沈着や結合組織の増生があり内腔は赤血球で充満している．さらに慢性の例では肺ヘモジデリン症を呈しうる．
　透過性亢進型肺水腫をきたす急性肺損傷（ALI）/急性呼吸促迫症候群（ARDS）では，原因によって差があるものの，組織学的に肺水腫，出血，硝子膜形成，好中球を主体とした細胞浸潤など，びまん性肺胞障害（diffuse alveolar damage：DAD）の像がみられる．
病態生理
　心原性とそれ以外の非心原性肺水腫に大別される．
　心原性肺水腫では肺の基本構造は保持されており，酸素吸入により低酸素血症は改善しやすい．肺うっ血を軽減するために起坐呼吸（orthopnea）となる．一方，非心原性肺水腫は基礎疾患によって病態生理が異なり，診断・治療に苦慮することが多い．急性呼吸促迫症候群（ARDS）などでは肺内シャントの病態を伴うことが多く，酸素投与によっても低酸素血症は改善しにくい．
臨床症状
　心原性肺水腫では喘鳴，呼吸困難，特に，発作性夜間呼吸困難や起座呼吸，咳および泡沫状のピンク色の痰が特徴である．身体所見では努力性呼吸，頻呼吸，頻脈，頸静脈の怒張がみられる．皮膚は蒼白で冷湿，チアノーゼを伴い，ショックに陥ることもある．聴診上，肺で水泡音（coarse crackle）が聴取される．
　ALI/ARDSは，非心原性肺水腫の大半を占める透過性亢進型肺水腫である．原因によって特異な臨床像を呈することが多い．表7-10-3に示す基礎疾患の経過中に，治療抵抗性の急性呼吸不全を呈し，胸部画像所見で両肺に浸潤影がみられる．
　神経原性肺水腫（neurogenic pulmonary edema）は，くも膜下出血，痙攣発作後など急性で重症の中枢神経系障害に伴う肺水腫である．おもな発症機序としては，脳室圧の上昇による交感神経系の関与が示唆されている．
　再膨脹性肺水腫（reexpansion pulmonary edema）は，気胸や胸水で虚脱した肺を急に再膨張させたときに発症する．虚脱の程度が重症で虚脱の期間が長いときにみられやすい．
　高地肺水腫（high-altitude pulmonary edema）は，心肺に異常のない健常人が2500 m以上の高地に急に到達した際に発症する．一般に高地に到達後2～3日以内に出現する．眼底出血や脳浮腫を合併することがある．低地移送で速やかに軽快する．
検査成績
　心原性肺水腫は，胸部X線では，肺胞性浸潤影（air space consolidation）を呈し，心拡大を伴うことが多い．心不全の悪化とともに血中BNP濃度が上昇する場合が多い．非心原性肺水腫の診断は，胸部X線写真ではときに困難であるが，胸部CTではすりガラス様陰影（ground glass opacity）を呈するが，心拡大は伴わない（図7-10-5）．なおいずれの肺水腫でも動脈血ガス分析では低酸素血症および呼吸性アルカローシスを呈する．
発症機序・鑑別診断
　臨床的に静水圧性および透過性亢進型を鑑別するには以下のような方法がある．
1）胸部画像診断：
心原性肺水腫では心陰影，肺血管影は拡大する．血管や気管支周囲には浮腫のため輪郭は肥厚し不鮮明（cuffing sign）となる．重症肺水腫では水腫影が両肺門から肺野の中心にかけて蝶形あるいは蝙蝠の羽（butterfly， bat’s wing）様を呈することがある．中心静脈圧が上昇すれば，上大静脈陰影が幅広くなり奇静脈も拡張する．胸水，特に右側優位がみられる．限局性の胸水貯留は腫瘤様でかつ治療により改善するのでvanishing tumorとよばれる（図7-10-6）．また，小葉間隔壁の浮腫によるKerley B 線がみられる．
　一方，透過性亢進型肺水腫では，心原性とは異なり，心拡大はなく肺血管影や上大静脈の拡大もみられない．
2）Swan-Ganzカテーテルによる肺動脈楔入圧（P_wp）の測定：
心原性か非心原性肺水腫を鑑別するために有用である．Forresterの分類では，P_wp≧18 mmHgのとき左心不全と定義されており，心原性肺水腫と診断する．
3）肺水腫液の解析：
肺水腫液が多く採取されれば，その細胞成分や生化学的解析により鑑別が可能である．たとえば，肺水腫液/血液の蛋白濃度比は，静水圧性では0.5以下，浸透圧亢進型では0.7以上である．
診断
　典型的な肺水腫の診断はその臨床像からは困難ではない．基礎疾患の推定も，先行する慢性の心疾患が存在する場合は容易であるが，心疾患のない場合は，重症の肺炎，肺塞栓症などとの鑑別が必要になることがある．
治療
　低酸素血症の改善，肺水腫に対する治療および原因疾患の治療が主体となる．　安静，半座位とし痰の喀出をはかる．P_aO₂ 60 torr（S_pO₂ 90％）以上となるように酸素吸入を行う．　肺水腫に対しては，透過性亢進型であっても，肺血管内圧を下げるのが基本である．心原性肺水腫に対しては利尿薬の投与をはじめとする心不全の治療が中心となる．透過性肺水腫であるALI/ARDSでは原因となった基礎疾患により治療法が異なる．［木村　弘］
■文献
Crandall ED, Staub NC, et al: Recent developments in pulmonary edema. Ann Intern Med, 99: 808-822, 1983.
Fraser RS, Colman N, et al: Synopsis of Disease of the Chest, 3rd ed, Elsevier, Philadelphia, 2005.

表7-10-3
肺水腫の分類">

表7-10-3

出典　内科学第10版内科学第10版について　情報

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