As a clinician, you are familiar with the concept of “pulmonary edema”, which literally means “expansion of the lung volume due to excess water in the lungs”. The textbook concept of pulmonary edema is “caused by the infiltration of fluid from the capillaries into the interstitial space or alveoli of the lungs”. There are several key words here: ① “fluid”, which means “basically water” implicitly; ② “capillary”, which means “from the blood vessels (2) “capillary”, meaning “from the blood vessel”, referring to the source; (3) “infiltration”, implying that the pores are small and can only slowly seep out, such as the use of “leakage”, referring to the larger pores and easy to flow out; (4) “interstitial or alveolar “, referring to the destination. In short, the meaning is very clear, pulmonary edema is “mainly water fluid”, “from the capillaries”, “slowly penetrate”, the destination is “lung interstitial or alveolar”. If the pulmonary edema gets worse, that is, if the capillary “pores” get “bigger”, all the other plasma components, except for the red blood cells, which are huge, leak out of these large capillary “pores “Leak out, the lung interstitium or alveoli will be filled with what is “plasma”, “plasma”, or “plasma”. At this point, the lung becomes something, water is replaced by plasma, called “pulmonary hematoma” it. But generally do not call it so, because the reason is unknown, to give it a medical common, with a strong color of simple materialism, is actually with the “garbage can” and “recycling bin” with the connotation of the magnificent term, “syndrome capillary leak syndrome”. Capillary leak syndrome is a term used in critical illnesses that physicians in other specialties may not be familiar with, so the clinical misdiagnosis rate is extremely high. The treatment of pulmonary edema is mainly to reduce the load, i.e., to reduce the pressure of internal extravasation of pulmonary capillaries (the pores are still small), while the treatment principle of capillary leakage syndrome is to “plug the leak” (the pores are too large), increasing the denseness of pulmonary capillaries has increased the main contradiction. Clinicians must be very familiar with this issue, which is a pathophysiology common to patients with multiple critical illnesses. Some relevant knowledge will be presented below for reference. I. Pulmonary edema The normal anatomical and physiological mechanisms within the lungs keep the interstitial fluid constant and the alveoli in an ideal moist state to facilitate the accomplishment of various pulmonary functions. If some causes cause an excessive increase in the amount of extravascular fluid in the lungs or even infiltration into the alveoli, it can be transformed into a pathological state called pulmonary edema (pulmonary edema). Clinical manifestations are dyspnea, cyanosis, cough, coughing of white or bloody foamy sputum, scattered wet rales in both lungs, and imaging presentation as butterfly or sheet-like faint shadows centered on the pulmonary hilum. The prognosis of this disease is closely related to the underlying pathology, the degree of pulmonary edema and the presence or absence of complications and proper treatment, and varies greatly among individuals. The concept of pulmonary edema is caused by the infiltration of fluid from the capillaries into the interstitium or alveoli of the lungs. The common clinical forms of pulmonary edema are cardiogenic pulmonary edema and nephrogenic pulmonary edema. Pathologically, they can be divided into two categories: interstitial and alveolar, and can coexist or be dominated by one category. Interstitial pulmonary edema is mostly chronic, and alveolar can be acute or chronic pulmonary edema. The etiology is mainly due to the infiltration of fluid from capillaries into the interstitial or alveolar lungs. The common clinical forms of pulmonary edema are cardiogenic pulmonary edema and nephrogenic pulmonary edema. The symptoms are mainly tachycardia, cough, frothy or pink blood sputum, dyspnea and even cyanosis. In humans, two types of pulmonary edema can occur that are fundamentally different in nature: cardiogenic pulmonary edema (also known as hydrostatic or hemodynamic pulmonary edema) and noncardiogenic pulmonary edema (also known as increased permeability pulmonary edema, acute lung injury, or acute respiratory distress syndrome). Despite their apparently different etiologies, the distinction between cardiogenic and noncardiogenic pulmonary edema can be difficult due to their similar clinical presentation. Defining the etiology of acute pulmonary edema is important for its treatment. Although the underlying cause of cardiogenic pulmonary edema may require additional treatment (including coronary revascularization), patients with this type of pulmonary edema usually receive diuretics and afterload reduction therapy. Patients with noncardiogenic pulmonary edema who require mechanical ventilation should be ventilated with low tidal volume (6 ml/kg expected body weight) and low airway pressure (<750pxh2o)< span="">. This lung-protective ventilation strategy reduces mortality in patients with acute lung injury. In addition, recombinant activated protein C and low-dose hydrocortisone should be considered for patients with severe sepsis. Noninvasive methods should be used to rapidly determine the etiology of acute pulmonary edema, and when the diagnosis is uncertain, adjunctive use of pulmonary artery cannulation can help to take timely and reasonable therapeutic measures. A proper diagnosis of acute pulmonary edema requires an understanding of fluid exchange in the microvasculature of the lungs. In the normal lung, fluid and protein leak out mainly through small gaps between capillary endothelial cells. Fluid and solutes that filter from the blood circulation into the alveolar spaces do not usually enter the alveoli because the connections between the alveolar epithelial cells are very tight. More precisely, once the filtered fluid enters the alveolar space, it asks to move proximally into the interstitial space around the bronchial vessels. Under normal conditions, most of the interstitial fluid can re-enter the body circulation via lymphatic reflux. The movement of plasma proteins with larger molecules is restricted. The hydrostatic pressure of fluid filtration in the pulmonary microcirculation is approximately equal to the hydrostatic pressure within the pulmonary capillaries, with some of the hydrostatic pressure within the pulmonary capillaries being offset by the protein osmolarity gradient. The rapid increase in fluid hydrostatic pressure within the pulmonary capillaries results in increased transvascular fluid filtration, a hallmark of acute cardiogenic or volume-load-increasing edema. The cause of elevated pulmonary capillary hydrostatic pressure is usually elevated pulmonary venous pressure, which in turn is often the result of elevated left ventricular end-diastolic and left atrial pressures. Mild elevations in left atrial pressure <18< span=""> to 25 mmHg) result in interstitial edema around microvessels and bronchial vessels. With further elevation of left atrial pressure (>25 mmHg), edematous fluid with low protein content breaks through the alveolar epithelium and pours into the alveolar cavity. In contrast, noncardiogenic pulmonary edema is the result of increased pulmonary vascular permeability, leading to an increased amount of fluid and protein entering the interstitial and air spaces of the lungs. The higher protein content of edema fluid in noncardiogenic pulmonary edema is due to increased filtration of plasma proteins as a result of increased vascular membrane permeability. The net retention of pulmonary edema fluid depends on the balance between the rate of fluid filtration and the rate of emigration from the air spaces and interstitial lung mass. II. capillary leak syndrome Capillary leak syndrome (CLS) is a sudden, reversible capillary hyperpermeability in which plasma rapidly permeates from the blood vessels into the tissue interstitium. It causes rapidly progressive systemic edema, hypoproteinemia, decreased blood pressure and central venous pressure, weight gain, hematoconcentration, and, in severe cases, multi-organ failure. The presence of capillary leak syndrome makes clinical treatment difficult and is one of the factors affecting the success of resuscitation. The treatment of capillary leak syndrome has certain special features, such as the water intake should be limited under the condition of ensuring circulation, too much rehydration can cause tissue interstitial edema, cellular edema, pulmonary edema aggravation, pericardial, thoracoabdominal exudation increase, aggravate organ function damage; especially in the recovery period, we should be alert to the pulmonary edema caused by large amount of fluid re-infiltration, appropriate diuresis to reduce the degree of pulmonary edema. Secondly, when raising the plasma colloid osmotic pressure, because the molecular weight of human serum albumin is 66 270 D, it can leak into the tissue interstitial space, and the colloid osmotic pressure of tissue interstitial space increases, so that more water accumulates in the tissue interstitial space. The effect of The mechanism of hydroxyethyl starch to prevent capillary leak is: (1) biophysical effect: hydroxyethyl starch has the right shape and size of molecular sieve to plug the leak; (2) biochemical effect: inhibit the expression of inflammatory mediators, reduce the release of pro-inflammatory mediators, prevent neutrophil adhesion, thus improving microcirculation, reducing the inflammatory response and endothelial damage. In addition, the use of small doses of glucocorticoids, equivalent to physiological doses, can improve capillary permeability and inhibit inflammatory responses, and can avoid hormone-induced hyperglycemia and related immunosuppression to a certain extent. Capillary leak syndrome (CLS) is a sudden, reversible capillary hyperpermeability in which plasma rapidly permeates from the blood vessels into the tissue interstices. It causes rapidly progressive systemic edema, hypoproteinemia, decreased blood pressure and central venous pressure, weight gain, hemoconcentration, and in severe cases, multi-organ failure. The presence of capillary leak syndrome poses difficulties in clinical treatment and is also one of the factors affecting the success of resuscitation. In this case, the patient aspirated a large amount of light red bloody fluid from the trachea for a considerable period of time, which is rare clinically; laboratory tests showed that its composition was close to that of plasma, indicating that there was a large amount of plasma components leaking from the lungs. It was also found for the first time that the amylase content in its respiratory exudate was significantly higher at 1550 U/L. The mechanism is unclear and may be related to the increased secretion of salivary amylase from the respiratory tract. Most of the patchy shadows in acute respiratory distress syndrome are peripherally distributed in the lungs, and the exudative shadows in acute pulmonary edema are mostly distributed centripetally. The chest X-ray of our patient showed diffuse patchy shadows in both lungs, but with a tendency for a centripetal distribution in the middle and lower lung fields. This appears to be a superposition of the two manifestations of acute respiratory distress syndrome and acute pulmonary edema on chest X-ray, and is also consistent with the pathophysiology of massive leakage of plasma components in capillary leak syndrome, so clinical attention should be paid to its recognition. The treatment of capillary leak syndrome has certain special features, such as the water intake should be limited under the condition of ensuring circulation, too much rehydration can cause tissue interstitial edema, cellular edema, pulmonary edema aggravation, pericardial, thoracoabdominal exudation increase, aggravate organ function damage; especially in the recovery period should be alert to the pulmonary edema caused by large amount of fluid re-infiltration, appropriate diuresis to reduce the degree of pulmonary edema. Secondly, when raising the plasma colloid osmotic pressure, because the molecular weight of human serum albumin is 66 270 D, it can leak into the tissue interstitial space, and the colloid osmotic pressure of the tissue interstitial space increases, so that more water accumulates in the tissue interstitial space, so less albumin should be used; the blood volume should be supplemented with artificial colloid, such as hydroxyethyl starch (Hers and Wanlin, the molecular weight of the former is 200 kD; the latter is 130 kD), capillary cannot leak into the tissue interstices when leaking. In addition, the use of small doses of glucocorticoids equivalent to physiological doses can improve capillary permeability, inhibit the inflammatory response, and avoid hormone-induced hyperglycemia and associated immunosuppression to some extent. Because of insufficient understanding of the pathophysiology of this patient at that time, hydroxyethyl starch was not applied in time to plug the leak, so the treatment effect was poor, which should attract clinical attention.