Acute respiratory distress syndrome

Introduction to acute respiratory distress syndrome Acute respiratory distress syndrome (ARDS) refers to acute, progressive, and hypoxic respiratory failure after traumatic, shock, and other intrapulmonary attacks. It is characterized by alveolar capillary damage and belongs to acute lung injury (acutelunginjury). , ALI) is a serious stage or type. Its clinical features respiratory rate and distress, progressive hypoxemia, X-ray showed diffuse alveolar infiltration. ARDS has many names, such as shock lung, diffuse alveolar damage, traumatic wet lung, and adult respiratory distress syndrome (ARDS). Its clinical features respiratory rate and distress, progressive hypoxemia, X-ray showed diffuse alveolar infiltration. This disease is quite similar to infant respiratory distress syndrome, but its etiology and pathogenesis are not the same. To distinguish, in 1972, Ashbauth proposed the name of adult respiratory distress syndrome (adultrespiratory distresssyndrome). It is now noted that the intrinsic nature also occurs in children. Therefore, European and American scholars have reached a consensus to discuss the accident, replacing the adult with an acute, called acute respiratory distress syndrome, and the abbreviation is still ARDS. basic knowledge The proportion of patients: the incidence of the original respiratory infection, the incidence rate of about 0.03% - 0.05% Susceptible people: no specific population Mode of infection: non-infectious Complications: renal failure, bacterial pneumonia, abscess, mediastinal emphysema, pneumothorax

Causes of acute respiratory distress syndrome

Shock (35%):

Due to the low blood volume caused by massive blood loss, the traumatic output can be reduced, and the blood flow of the lungs is also reduced. Due to the decrease of pulmonary blood volume and the continuous insertion of microemboli from the systemic circulation, the pulmonary vascular bed can be blocked. , which hinders the progress of gas exchange, and the contraction of bronchial and pulmonary small blood vessels caused by damaged blood cells and tissue decomposition products, which can increase capillary permeability, cause pulmonary interstitial congestion, edema, increase respiratory resistance, and thus last for a long time. On the basis of sexual shock, plus other factors, such as a large number of infusions, blood transfusions, etc., can lead to respiratory distress syndrome.

Fat embolism (25%):

Fat embolism is a common complication after multiple fractures. Large fat droplets can block the pulmonary arterioles and expand them. Small fat droplets can be dispersed in many tiny blood vessels, causing extensive microcirculation embolism, while neutral fat is in lipase. Under the action, it is decomposed into free fatty acids, which causes chemical inflammatory reactions, which can lead to pulmonary edema and pulmonary hemorrhage. It is clinically characterized by hypoxemia and is an important indicator of lung function damage.

Too much infusion (10%):

In severely traumatized people, due to the stress response, the reaction time of water and salt retention is relatively long, often exceeding 72 hours. Therefore, a large amount of infusion after the injury can leave a few liters of water in the body, expanding the amount of extracellular fluid, and a large amount of electrolyte solution. It can also dilute plasma protein, reduce the colloid osmotic pressure of plasma, and promote pulmonary edema. In addition, if the lung itself is directly damaged by various reasons, such as contusion, aspiration, shock or sepsis, it is more normal than normal lung. It is easier to retain water, so even a slight infusion is prone to pulmonary edema. Therefore, excessive infusion is a very important factor in many factors of acute respiratory distress syndrome. Some authors have studied pulmonary edema in dogs. The difference in hydrostatic pressure between the extremities, the small intestine and the pulmonary capillaries was found to be edema when the capillary pressure of the limbs was 16 mmHg and the capillary pressure of the small intestine was 15.4 mmHg. Pulmonary edema occurred when the pulmonary capillary pressure was 7.6 mmHg.

Infection (5%):

Suppurative infection can cause bacterial toxins or cell rupture products to enter the pulmonary circulation. Under the action of endotoxin, vasoactive substances such as 5-hydroxylamine, histamine acetylcholine and catecholamine can be released in the body, which can increase capillary permeability and infection. It can also be transferred to the lungs, which can lead to pulmonary failure. In shock, multiple trauma and massive infusion, it is easy to cause sepsis in patients.

Traumatic brain injury (3%):

Severe craniocerebral trauma is often complicated by pulmonary edema. This is because brain trauma can stimulate strong sympathetic impulses, leading to significant peripheral vasoconstriction, followed by acute heart failure and pulmonary edema. If -adrenergic blockers are used in advance, This damage can be prevented. Recently, it has been found that the protein content in the effusion of post-traumatic pulmonary edema is high, so in addition to hypertensive edema, there may be a factor of permeability edema.

Aspiration (2%):

As a cause of respiratory distress syndrome, aspiration has recently received attention. It is very serious to aspirate a large amount of acidic stomach contents. A small amount of acidic secretions with a pH lower than 2.5 can also cause serious consequences, causing chemistry. Pneumonia and lung infections, which lead to respiratory failure.

Oxygen poisoning (1%):

In respiratory failure, high-concentration oxygen is often used, but long-term use causes lung damage. The main factors that determine oxygen poisoning are the pressure of inhaled oxygen and the time of oxygen inhalation. The greater the inhaled oxygen pressure, the longer the time, the possible damage of oxygen to the body. The larger the lung oxygen poisoning, the cilia ciliary movement can be significantly inhibited, 100% oxygen inhalation for 6h, can produce asymptomatic acute bronchitis, Sevitt through a large number of autopsy, that the transparent membrane and proliferative pneumonia as human lung The main pathophysiological changes of oxygen poisoning are ventilatory-perfusion imbalance, a large amount of blood flowing through the lungs, edema, ablation, mutation and fibrosis, resulting in a significant increase in physiologic shunt in the lungs. Therefore, persistent hypoxemia occurs, and there is a gas diffusion disorder in the late stage, and the carbon dioxide discharge is blocked. Even if the high concentration of oxygen is inhaled, the arterial oxygen partial pressure cannot be increased, and only the toxicity damage to the lung can be aggravated. Animals often die from severe hypoxic heartbeats.

The etiology of ARDS is based on the nature, and each category has several diseases or pathogenic factors.

The etiology of ARDS varies, but the pathophysiology and clinical process are basically independent of the specific cause. The common basis is acute damage to the alveolar-capillary. The lung injury can be direct, such as inhalation of stomach acid or toxic gas, chest and wounds. Etc. causes physicochemical damage to the endothelium or upper cells, and more often refers to indirect lung injury. Although the mechanism of lung injury has not been fully elucidated so far, it has been confirmed to be part of the systemic inflammatory response syndrome in alveolar capillaries. An acute inflammatory response mediated by cells and body fluids, involving two major processes, the migration and aggregation of inflammatory cells, and the release of inflammatory mediators, which complement each other and act on specific components of the alveolar capillary membrane, resulting in permeability. Increase.

Pathogenesis

So far, the mechanism of eigengenesis is still not clear. Some of the following mechanisms that have been envisioned by scholars have not explained all the morbid conditions. The incidence of each specific patient often needs to be clarified by several mechanisms.

1. Pulmonary edema trauma, shock and various pathogenic factors make the pulmonary circulation insufficient blood perfusion, can directly damage the alveoli and capillaries, caused by various damage media, such as microthrombus, vasoactive substances or inflammatory mediators The damage of the alveolar-capillary membrane increases the permeability, and the fluid can leak from the capillaries into the alveoli or interstitium, causing pulmonary edema. In addition, shock, trauma or other pathogenic factors cause insufficient cerebral perfusion. The brain metabolism is reduced, and the reflex pulmonary vasospasm is generated, which causes an increase in pulmonary venous pressure, and an infusion excess also accelerates pulmonary edema.

It has been observed that granulocytes in the blood circulation, platelets and tissue macrophages contain various inflammatory mediators, such as lysosomal hydrolases and phospholipases of granulocytes. When they are released into the pulmonary circulation, they can make alveolar capillaries. The vascular membrane produces extensive damage, which increases permeability, and proteins, blood cells and fluids can leak out of the blood vessels. At the same time, platelets can decompose histamine, serotonin and kinins, shrinking vascular endothelial cells, widening the intercellular space, and protein. Such as easy to seep, it is also conducive to the formation of pulmonary edema.

At first, the edema fluid only appeared in the interstitial tissue around the pulmonary arterioles, and gradually increased to the respiratory bronchioles. Finally, the entire alveoli were filled, and the ventilation/blood perfusion ratio was imbalanced to form hypoxemia.

2. Microthrombus formation in the lungs Solliday et al believe that various damage factors may increase the amount of catecholamines in the body, and sometimes cause an increase in iatrogenic catecholamines during the treatment. The increase of catecholamines is beneficial to induce platelet aggregation and form microthrombus. When they flow to the lungs, they can block the small arteries of the lungs, causing pulmonary circulatory disorders. Agglutinated platelets can also release serotonin and histamine, which can cause bronchospasm, affecting the ventilatory function of the lungs. When thrombosis occurs, fibrinogen is converted to In fibrin, vasoactive peptides are also released, which can increase local vascular and bronchospasm, increase pulmonary hypertension, increase alveolar capillary permeability, and produce alveolar and interstitial hemorrhage, edema, and alveolar fibrin deposition. In addition, embolization can affect the blood flow of pulmonary vascular blood vessels, causing the destruction of lung tissue structure, and finally reduce lung compliance, resulting in respiratory distress syndrome, but Malik et al believe that microthrombus must exist simultaneously with intravascular coagulation. Respiratory distress syndrome can occur.

3. Reduction of alveolar surfactant production When respiratory distress syndrome occurs, type I alveolar epithelial cells are often damaged, and its destruction not only seriously impairs the integrity of alveolar capillaries in the vascular barrier, but also must be type II epithelium. Cell differentiation replaces the damaged type I epithelial cells, so it directly affects the quantity and quality of alveolar surfactant. In addition, due to alveolar edema fluid filling, the activity of alveolar surfactant is also reduced, alveoli will tend to shrink, so the lungs The capacity can be reduced, resulting in difficulty breathing.

The respiratory distress syndrome that occurs after trauma, surgery or other diseases often has a certain incubation period. The half-life of the surfactant is 18 to 24 hours, and the two are similar in time. Therefore, some people think that the occurrence of respiratory distress syndrome is due to the surface. Reduced production of active substances.

4. The pathological basis of ARDS is pulmonary capillary membrane damage caused by a variety of inflammatory cells (macrophages, neutrophils and lymphocytes) mediated by local inflammatory reactions and inflammatory responses. The pathological feature is the formation of protein-rich pulmonary edema and transparent membrane in the alveolar exudate caused by increased pulmonary microvascular permeability, which may be associated with pulmonary interstitial fibrosis.

In the first 18 hours after the onset of clinical symptoms, the lungs were generally not significantly, with only a small amount of scattered hyperemia and atelectasis. After 18 to 72 hours after shock, the lesions were severe, showing a hemorrhagic lesion in the entire lung. Severe pulmonary venous congestion, scattered thromboembolism, interstitial edema, vascular and peri-bronchial hemorrhage and alveolar hemorrhage. 72 hours later, clear membrane and bronchial pneumonia were observed, followed by diffuse fibrosis, and exudative proliferative changes were simultaneously The existence of phase, the characteristics of pathological changes can be summarized as follows:

(1) Exudation period (2448h): alveolar and interstitial edema, capillary congestion, type I alveolar cell destruction, early transparent membrane formation, edema fluid protein content and composition similar to plasma, pulmonary microvascular endothelial cells It is roughly intact, and there is no gap at the junction of cells. However, red blood cells can be found in the interstitium, suggesting a short leak in the pulmonary microvascular endothelium. It may be due to the strong repair ability of endothelial cells, making the transient damage of the endothelial layer difficult to be find.

(2) Cell proliferative phase (3-7 days): Type II cells proliferate, inflammatory cells infiltrate the lung septum, and the hyaline membrane is mechanized. After the exudation period, the type II cells begin to proliferate rapidly as an initial repair reaction. The underlying disease is not controlled and produces sustained damage stimuli. In this period, neutrophils attach to the surface of pulmonary vascular endothelial cells, and pulmonary vascular microthrombus formation. The changes of lung parenchyma are characterized by thickening of the epithelial layer and obvious interstitial Swelling, microvessels are greatly reduced or collapsed by compression, and the interstitial enlargement in this period is due to edema and cell proliferation.

(3) Fiber proliferative phase (>7-10 days): fibrosis of hyaline membrane and alveolar septum, alveolar duct fibrosis.

(4) Microscopic examination: alveolar expansion, alveolar pores increased significantly, capillaries in the alveolar wall were more clear, some type I alveolar and capillary endothelial cells were swollen, fibrin, platelets, red blood cells were seen in alveolar capillaries And leukocyte accumulation, in most lung tissues, white blood cells increased significantly. On the surface of red blood cells and alveolar cells, cellulose-like substances were observed. The nuclear chromatin of type II cells became thick, the perinuclear space was widened, and mitochondria were disordered or disappeared. The expansion of the plastid network, the destruction of the lamellar structure or the emptying phenomenon, so there are vacuoles of different sizes in the cytoplasm of type II cells. In the alveolar cavity, free or agglomerated white blood cells, red blood cells, macrophages and Exfoliated type II cells, some alveolar cavities are also covered with edema fluid or other mucus-like secretions, the interstitial space of the interstitial part of the lung is widened, and edema may occur to varying degrees. Occasionally, the elastic fibers and collagen fibers are sparsely arranged and disordered. The alveolar structure is blurred and the boundary is unclear. The surface of alveolar epithelial cells can be covered by criss-crossing cellulose.

(1) Migration and aggregation of inflammatory cells Almost all intrapulmonary cells participate in the pathogenesis of ARDS to varying degrees, and polymorphonuclear leukocytes (PMNs), one of the most important effector cells of acute inflammation of ARDS, are isolated and isolated. There are only a small amount of PMNs in the mass, accounting for 1.6%, in trauma, sepsis, acute pancreatitis, physical and chemical stimulation or extracorporeal circulation, due to endotoxin lipopolysaccharide (LPS), C5a, interleukin-8 (IL) -8) Other factors, PMNs accumulate in the capillary capillaries, firstly the Coanda flow and adhere to the endothelial cells, and then transend the endothelium to the pulmonary interstitial, and then moved to the alveolar space by alveolar epithelial desquamation, which In a process, there are many kinds of adhesion molecules involved in the regulation and regulation. The respiratory outburst and release of PMNs are important links of lung injury. Alveolar macrophages (AMs) are also inflammatory reactions in addition to phagocytic cells and antigen-presenting cells of immune response. The important effector cells involved in the pathogenesis of ARDS, stimulated and activated AMS release IL-1, tumor necrosis factor- (TNF-) and IL-87, etc., which promotes chemotaxis and aggregation of PMNs in the lung is likely to be the initiation of ALI. Factor, platelet aggregation And microembolism is a common pathological change of ARDS. It is speculated that platelet aggregation and microembolism are common pathological changes of ARDS. It is speculated that platelets and their products play an important role in the mechanism of ARDS. In recent years, structural cells such as pulmonary capillaries and alveolar epithelial cells have been found. Not only the target cells, but also participate in the inflammatory immune response, which has special significance in the secondary inflammatory response of ARDS.

(B) the release of inflammatory mediators The activation and release mediators of inflammatory cells are accompanied by the same inflammatory response, which is inseparable. It is discussed separately for convenience of description. Take bacterial LPS stimulation as an example, which binds to macrophage surface receptors. Cell shedding and cell gadgets release numerous media, including:

1 lipid medium such as arachidonic acid metabolite, platelet activating factor (PAF);

2 Reactive oxygen metabolites include superoxide anion (O2-), hydrogen peroxide (H2O2), hydroxyl radical (OH·) and monomeric oxygen (IO2). In addition to H2O2, symmetric oxygen itself is exaggerated, and 3 peptides such as PMNs/AMs proteases, complement substrates, various components involved in the process of coagulation and fibrinolysis, cytokines, and even integrins that belong to the adhesion molecule steroids are also listed in such media.

(iii) Alveolar Capillary Damage and Increased Permeability The components that maintain and regulate capillary structural integrity and permeability include extracellular matrix, intercellular junctions, cytoskeleton, and interactions between pinocytic transport and cellular substrates, ARDS Direct and indirect damage can affect each of the above steps, oxygen self-base, protease, cytokines, arachidonic acid metabolites and high-charged products (such as neutrophil major cationic protein) can be obtained through the following pathways Altering the permeability of the membrane barrier; (1) lysing the basement membrane protein and/or cell adhesion factor; (2) altering the extracellular matrix of the extracellular matrix; and (3) affecting the fibril system of the cytoskeleton, resulting in cell deformation and tearing of the junction.

Pathophysiology

(1) The basic pathophysiology can be expressed in Figure 1. It should be pointed out that the damage and pathological changes of ARDS are generally considered to be diffuse. In recent years, studies on the exchange of gas from imaging and application of inert gas have shown that lung injury It is not as diffuse and uniform as it was understood in the past, so a two-compartment model is proposed: one room is a near-normal lung, and there is no difference in the pressure and ventilation response applied to it; the second chamber is the diseased lung, its expansion and Ventilation is reduced, but disproportionate blood flow is received. In the early two chambers, many open lung units can be exchanged as the applied pressure increases or the position changes, so the apparent pressure- curve is significantly lagging and biphasic. Morphology, early pulmonary edema reduces alveolar volume, in a sense, only the volume of filling is reduced, rather than the lung volume itself, the total lung and thoracic volume in the functional residual position are in the normal range, specific lung compliance ( Specific compliance) Compliance/Lung volume is also normal.

(2) Oxygen consumption - pathological dependence of oxygen supply and multiple organ failure

In recent years, some studies have found that there is an abnormal relationship between oxygen consumption and oxygen supply (Vo2Qo2) in ARDS, and that this common pathophysiological basis of ARDS and multiple organ failure, healthy human oxygen supply can change, even if reduced, and organ oxygen Intake and consumption remain relatively stable, that is, the oxygen consumption of the organ is not dependent on oxygen supply above the critical threshold, but is due to local compensatory effects and increased capillary perfusion and increased oxygen uptake. This compensation mechanism in ARDS Depletion, the absolute dependence or pathological dependence of oxygen consumption on oxygen supply occurs at all oxygen supply levels (Fig. 2). This pathological phenomenon shows VA/Q ratio imbalance in the lung and tissue and capillaries in the extrapulmonary organs. Inter-oxygen exchange disorder, abnormal Vo2/Qo2 relationship leads to cell oxygenation and metabolic disorders, causing damage. The imbalance of oxygen supply and demand stems from the depletion of local compensatory mechanism. The explanation is that redistribution of blood flow to low-lying organs such as skeletal muscle. , causing the need for vital organ oxygen supply; another kind of cleanliness is the capillary damage of vital organs, tissue edema, increased diffusion distance and reduced hair cell cross-sectional area, causing damage The basic reason is the general activation of inflammatory cells and the release of mediators. At present, it tends to the latter view. It is believed that ARDS and multiple organ failure have a common pathogenesis. Because of the abundant abundant capillary beds, it is often the first target of inflammatory damage. Organs, the early rescue of ARDS is effective or causes the cause of systemic inflammatory response is self-limited or controlled, the disease course only shows ARDS without multiple organ failure, ARDS develops or evolves into multiple organ failure, infection may be the most important trigger Or the driving factor.

[pathological changes]

The pathological changes of ARDS caused by various causes are basically the same, which can be divided into three interrelated and partially overlapping stages of exudation, hyperplasia and fibrosis.

(1) The exudation period is seen in the first week after the onset of the disease. The lungs are dark red or dark purple liver-like changes. The edema, hemorrhage, and weight increase are obvious. The microscopic blood vessel congestion, hemorrhage, microthrombus, and lungs are observed within 24 hours. There is protein edema and inflammatory cell infiltration in the interstitial and alveolar. If it is caused by a sensible cause, the accumulation and infiltration of PMNs in the alveolar cavity is more obvious. After 72 hours, the plasma protein is coagulated, the cells are fragmented, and the cellulose forms a transparent membrane. Sexual or large alveolar atelectasis, impaired necrosis of type I cells during acute exudation.

(2) 1 to 3 weeks after the proliferative injury, the type II lung epithelial cells proliferate and cover the basement membrane of exfoliation, fibrosis can be seen in the alveolar sac and alveolar duct, and fibrocytic intimal hyperplasia occurs in the muscular small arteries, resulting in the cross-sectional area of the vascular lumen. cut back.

(3) The alveolar septum and the air wall of the ARDS patients with fibrosis survival for more than 3 to 4 weeks were extensively thickened, diffuse irregular fibrosis caused by the separation of collagen connective tissue, and extensive wall fiber thickening occurred in the pulmonary vascular bed. Distorted arterial deformation, vasodilation of the lungs, even if the ARDS caused by non-infectious causes, in the later stages, inadvertently combined with pulmonary infection, tissue necrosis and microscopic abscesses are common.

Acute respiratory distress syndrome prevention

Patients with high-risk should be closely observed and intensively monitored. Once the respiratory rate is low, PaO2 is lowered, and other lung injury manifestations are observed. When the primary treatment is open, respiratory support and other effective prevention and intervention measures should be given early to prevent further development of ARDS. And important organ damage.

The prognosis of ARDS is related to the primary disease, complications and response to treatment. However, if the sepsis caused by severe infection is not controlled, the prognosis is very poor. The bone marrow transplantation is complicated by ARDS death. The rate is almost 100%. If the prognosis of multiple organ failure is extremely poor, and it is related to the number and speed of affected organs, such as 3 organ failures lasting more than 1 week, the mortality rate can be as high as 98%. After active treatment, If the continuous pulmonary vascular resistance increases, indicating a poor prognosis, ARDS caused by fat embolism, after active treatment, mechanical ventilation can achieve 90% survival, acute pulmonary edema and ARDS caused by irritating gas, generally off the scene, timely treatment, Can also achieve better curative effect, another ARDS patients treated with PEEP0.98 (10cmH2O), PaO2 increased significantly, the prognosis is good, most patients with ARDS can be quickly relieved, most of them can return to normal, 40% of pulmonary dysfunction Among the ARDS restorers, 20% showed obstructive ventilatory damage, 30% decreased diffuse, and 25% decreased PaO2 during exercise.

Once ARDS is present, the prognosis is more serious, the treatment is complicated and difficult, and the important thing is prevention and early treatment. ARDS is usually used as part of the systemic multiple organ dysfunction syndrome. In clinical practice, it is difficult to see simple ARDS while the patient does not merge with other patients. Organ dysfunction, in fact, most patients with ARDS are caused by extrapulmonary dysfunction or trauma, infection, etc., and then cause dysfunction of the lung itself, further leading to lung infection, which in turn aggravates the disease of ARDS, so ARDS Treatment as part of the systemic multiple organ dysfunction syndrome is the basic concept of successful ARDS treatment. For shock and severe trauma patients, the following points should be noted:

1 rapid recovery of circulating blood volume after shock occurs; 2 retain the airway catheter until the patient is fully awake and adequate ventilation;

3 actively encourage patients to take deep breaths;

4 often change position;

5 Where the transfusion exceeds 4 units, it should be filtered using a standard filter, and excessive infusion of stale stock blood should be avoided as much as possible;

6 supplementary nutrition;

7 control excessive and too fast infusion;

8 should not be too long for pure oxygen, it is best to apply 40% oxygen;

9 to prevent gastric juice from inhaling into the lungs, especially for patients who are conscious of coma.

Complications of acute respiratory distress syndrome Complications, renal failure, bacterial pneumonia, abscess, mediastinal emphysema, pneumothorax

Shortly after the illness in patients with acute respiratory distress syndrome, if the condition does not resolve after several days or weeks, complications of other organs may occur due to insufficient oxygen supply. Excessive hypoxia may cause serious complications such as renal failure. If not treated promptly, it may die due to severe hypoxia. Because of the low ability of patients with acute respiratory distress syndrome to prevent lung infection, bacterial pneumonia often occurs during the disease, chest complications such as abscess, mediastinum Emphysema and pneumothorax.

Symptoms of Acute Respiratory Distress Syndrome Common Symptoms Lifting Shoulder to Help Respiratory Cardiogenic Respiratory Distress Breathing Discomfort Hypoxemia Lung Texture Increase Respiratory Alkalosis Lip Hair Bleeding Respiratory Failure Carbon Dioxide Retention

In addition to the corresponding signs of the disease, when the lungs have just been damaged within a few hours, the patient may have no respiratory symptoms, then the respiratory rate is accelerated, the airlift is gradually aggravated, the lung signs are not abnormally found, or the inhalation can be heard. When the small wet voice, X-ray chest showed clear lung field, or only the lung texture increased fuzzy, suggesting that the blood around the blood vessels gather, arterial blood gas analysis showed that PaO2 and PaCO2 are low, as the disease progresses, the patient breathe distress, feel the chest Tight bundle, inhalation effort, purpura, often accompanied by irritability, anxiety, extensive interstitial infiltration of both lungs, may be accompanied by azygdal vein dilatation, pleural reaction or a small amount of effusion, due to hyperventilation caused by hyperventilation, PaCO2 decreased Respiratory alkalosis, respiratory distress can not be improved with the usual oxygen therapy, such as the above conditions continue to deteriorate, respiratory distress and purpura continue to increase, chest X-ray shows that the lungs infiltrated the vaginal large-scale fusion, and even developed into "white lung" Respiratory muscle fatigue leads to inadequate ventilation, carbon dioxide retention, mixed acidosis, cardiac arrest, and multiple organ failure in some patients.

The onset is more rapid, and the typical clinical process can be divided into 4 phases.

1. In the injury period, the main pathological manifestations were mainly 4 to 6 hours after injury, and the breathing could be increased quickly, but there was no typical respiratory distress, and no positive findings were found on X-ray films.

2. Relative stable period 6~48h after injury, after active treatment, the circulation is stable, and gradually dyspnea, frequency is accelerated, hypoxemia, hyperventilation, PaCO2 is reduced, lung signs are not obvious, X-ray chest radiograph is visible Increased texture, blurred and reticular infiltrates, suggesting increased accumulation of interstitial fluid and interstitial edema in the pulmonary vessels.

3. Respiratory failure period 24 to 48 hours after injury, difficulty breathing, distress and cyanosis, conventional oxygen therapy is invalid, can not be explained by other primary cardiopulmonary diseases, respiratory rate can be accelerated up to 35 ~ 50 times / min, chest auscultation can Smell and wet sputum, X-ray chest radiographs have scattered patchy shadows or ground glass-like changes, visible bronchial aeration sign, blood gas analysis PaCO2 and PaCO2 are reduced, often represented by acid.

4. Extreme end-stage dyspnea and severe cyanosis, neuropsychiatric symptoms such as drowsiness, paralysis, coma, etc. X-ray chest showed fusion into a large infiltrating shadow, bronchial aeration sign was obvious, blood gas analysis severe hypoxemia, CO2 Detention, there is often a mixed acid-base imbalance, and eventually circulatory failure can occur.

Examination of acute respiratory distress syndrome

Laboratory inspection

(a) lung function test

1. The lung volume and lung capacity are measured by the spirometer. The residual gas and functional residual gas are reduced, and the respiratory dead space is increased. If the dead volume/tidal volume (VD/VT) is >0.6, it indicates that mechanical ventilation is required.

2, lung compliance measurement: often measured at the bedside for total lung and lung compliance, patients with end-expiratory positive pressure ventilation, can be calculated according to the following formula dynamic compliance (Cdyn) compliance test not only for diagnosis, judgment Efficacy, and has practical value for monitoring the presence or absence of complication such as pneumothorax or atelectasis.

3, arterial blood gas analysis PaO2 reduction, is a common indicator of ARDS diagnosis and monitoring, according to arterial blood oxygen analysis can calculate the alveolar arterial oxygen pressure difference (PA-aO2), static arterial blood shunt (Qs / Qt), respiratory index ( Derived indicators such as PA-aO2/PaO2) and oxygenation index (PaO2/FiO2) are very helpful in diagnosing and evaluating the severity of the disease. For example, Qs/Qt increase is advocated for disease classification, which is higher than 15%, 25%. And 35% are divided into light, medium and heavy severity, the respiratory index reference range is 0.10.37, >1 indicates that the oxygenation function is significantly reduced, >2 often requires mechanical ventilation, and the oxygenation index reference range is 53.2-66.7kPa ( 400500mmHg), decreased to 26.7kPa (20mmHg) in ARDS, decreased arterial oxygen partial pressure (PaO2) when breathing air (60mmHg or 8.0kPa); arterial oxygen partial pressure (PaO2)/oxygen concentration (FiO2)300mmHg Or 200mmHg, normal arterial blood carbon dioxide partial pressure (PaCO2) normal or low, and respiratory alkalosis; late PaCO2 increase and respiratory acidosis, or combined with metabolic and / or respiratory acidosis, alveolar - Arterial oxygen partial pressure difference [P(Aa)O2] is still >26.6 kPa (200 mmHg) after 15 min of pure oxygen absorption, lung flow rate Up to 10%.

1. Determination of lung edema fluid protein ARDS, pulmonary capillary permeability increased, water and macromolecular protein into the stroma or alveolar, so that the ratio of protein content of edema fluid to plasma protein content increased, if the ratio of > 0.7, consider ARDS, <0.5 is cardiogenic pulmonary edema.

2, alveolar-capillary membrane permeability (ACMP) determination using dual-nuclear in vivo labeling technology, 113 indium (113In) autologous labeled transferrin, used to determine the amount of protein accumulation in the lung, while 99m (99mTc) autologous Labeling red blood cells, correcting the influence of blood flow distribution in the chest, calculating the ratio of pulmonary heart radiation count of 113 indium and 99m respectively, and observing the change of 2 hours to obtain the plasma protein accumulation index. The reference value of healthy people is 0.138×10-3/min. .

3. Hemodynamic monitoring Pulmonary arterial pressure (PAP), pulmonary capillary wedge pressure (PCWP), pulmonary circulation resistance (PVR), PVO2, CVO2, Qs/Qt and heat can be measured and calculated simultaneously by introducing a four-chamber floating catheter. Dilution of cardiac output (CO), etc., is not only valuable for diagnosis and differential diagnosis, but also for mechanical ventilation therapy, especially the effect of PEEP on circulatory function. It is also an important monitoring index. The mean arterial pressure of ARDS patients is increased by 2.67. kPa, pulmonary artery pressure and pulmonary capillary wedge pressure difference (PAP-PCWP) increased (>0.67kPa), PCWP is generally <1.18kPa (12cmH2O), if >1.57kPa (16cmH2O), it is acute left heart failure, can exclude ARDS .

4, pulmonary extravascular water content determination is currently measured by dye double trace dilution method, from the central vein or right heart catheter tube 5ml guanidine green dye glucose solution 10ml, and then recorded in the femoral artery through the catheter connected to the thermistor Diluting the curve, and using the densitometer to detect the dye dilution curve and then calculating the amount of lung water by computer processing, can be used to determine the degree of pulmonary edema, outcome and efficacy, but certain equipment conditions are required.

5, pulmonary artery wedge pressure acute lung injury and acute respiratory distress syndrome patients with pulmonary artery wedge pressure (PAWP) are lower than 18mmHg (2.40kPa) and secondary to pulmonary microcirculation venous pressure increased pulmonary edema patients, PAWP often 20mmHg (2.70 kPa), which is helpful for the exclusion of cardiogenic or volumetric pulmonary edema, but the pulmonary wedge pressure test is somewhat traumatic. Clinically, it is usually based on medical history, physical examination, X-ray and non-invasive examination methods (such as echocardiography). A preliminary judgment is made, and if necessary, a floating catheter is used to check the pulmonary wedge pressure.

Film degree exam

1. Chest X-ray showed chest X-ray plain film showed mild interstitial changes in the early stage, followed by patchy appearance, resulting in large-scale fusion shadows. The late two lungs showed extensive consolidation, combined with stubborn hypoxemia, for diagnosis. Great help, chest X-ray examination can help individual cardiogenic pulmonary edema and find related complications such as lung infection and pneumothorax.

2, chest computed tomography (CT) is also very helpful in the diagnosis of ARDS, more clearly showing the extent and location of the lesion, as well as chest complications found in chest X-ray films, such as abscess, mediastinal emphysema and pneumothorax, Repeated chest CT examination, especially in patients with ineffective conventional support or mechanical ventilation therapy, may provide important reference for finding the cause and adjusting the treatment. However, CT examination of such patients should pay attention to safe operation. After the recovery, chest CT examination can help to further understand Residual lesions in the lungs.

3, fiberoptic bronchoscopy fiberoptic bronchoscopy can be used for bronchoalveolar lavage (BAL), taking lavage fluid for neutral cell count and other indicators of inflammatory mediators, may be helpful in judging the condition, but still need clinical observation, The respiratory tract secretion can also be removed by fiberoptic bronchoscopy for pathogen detection to avoid contamination of the specimen by the upper respiratory tract colony.

Diagnosis and diagnosis of acute respiratory distress syndrome

diagnosis

Up to now, due to the lack of specific detection indicators, it has brought difficulties to early diagnosis. Any basic diseases or incentives that may cause ARDS, once respiratory changes or blood gas abnormalities occur, should be alert to the possibility of intrinsic occurrence, establish a comprehensive clinical diagnosis. , laboratory and auxiliary examinations, necessary dynamic follow-up observations, and exclusion of other diseases of similar performance, for disease statistics and scientific research needs, must be based on established diagnostic criteria, various diagnostic criteria have been proposed over the years, very different European and American scholars discussed in the academic conferences in the United States and Europe in 1992, and the definitions and diagnostic criteria for ALI and ARDS published in various magazines in 1994 and published in various magazines in 1994 have recently been widely introduced and recommended in China.

ARDS diagnostic criteria

Except for the specified PaO/FiO 26.7 kPa (200 mmHg), the other indicators are the same as ALI.

In 1995, the National Conference on Critical and Critical Emergency Education (Lushan) proposed the diagnostic criteria for ARDS staging in China according to the above criteria:

1. There is a primary cause of ARDS.

2. The diagnosis of a priori ARDS should have three of the following five items:

(1) Respiratory frequency 20 to 25 beats / min.

(2) (FiO20.21) PaO2 9.31 kPa ( 70 mmHg), > 7.8 kPa (60 mmHg).

(3) PaO2/FiO2 39.9 kPa ( 300 mmHg).

(4) PA-aO2 (FiO20.21) 3.32 to 6.65 kPa (25 to 50 mmHg).

(5) The chest radiograph is normal.

3. The diagnosis of early ARDS should have 3 out of 6 items.

(1) Respiratory rate > 28 beats / min.

(2) (FiO20.21) PaO2 7.90 kPa (60 mmHg) > 6.60 kPa (50 mmHg).

(3) PaCO2 < 4.65 kPa (35 mmHg).

(4) PaO2/FiO2 39.90 kPa ( 300 mmHg) > 26.60 kPa (> 200 mmHg).

(5) (FiO21.0) PA-aO2>13.30 kPa (>100 mmHg) <26.60 kPa (<200 mmHg).

(6) Chest radiograph shows no alveolar consolidation or consolidation 1/2 lung field.

4. The diagnosis of advanced ARDS should have 3 of the following 6 items:

(1) Respiratory distress, frequency > 28 beats / min.

(2) (FiO20.21) PaO2 6.60 kPa ( 50 mmHg).

(3) PaCO2>5.98 kPa (>45 mmHg).

(4) PaO2/FiO2 26.6 kPa ( 200 mmHg).

(5) (FiO21.0) PA-aO2>26.6 kPa (>200 mmHg).

(6) Chest radiograph shows alveolar consolidation 1/2 lung field.

Differential diagnosis

The disease must be differentiated from large insufficiency, spontaneous pneumothorax, upper respiratory airway obstruction, acute pulmonary congestion and cardiogenic pulmonary edema. The medical history and chest X-ray examination can be used to identify the disease.

1. Cardiac pulmonary edema (left heart failure) Acute respiratory distress syndrome is a non-cardiogenic pulmonary edema caused by alveolar capillary membrane damage and increased vascular permeability, and therefore must be due to factors such as increased hydrostatic pressure Cardiac pulmonary edema caused by cardiogenic pulmonary edema is common in hypertensive heart disease, coronary heart disease, cardiomyopathy, left heart failure and left atrial dysfunction caused by mitral stenosis They have a history of heart disease and corresponding clinical manifestations. For example, combined with chest X-ray and electrocardiogram, the diagnosis is generally not difficult. Cardiac catheter pulmonary capillary wedge pressure (Paw) rises in left heart failure (Paw>2.4kPa), Diagnostics make more sense.

2. Acute pulmonary embolism is more common in patients with postoperative or long-term bed rest. The thrombus comes from the deep vein or pelvic vein of the lower extremity. The onset of the disease is sudden, and there are breathing difficulties, chest pain, hemoptysis, cyanosis, PaO2 decline, etc., and ARDS is difficult to identify, blood. Increased lactate dehydrogenase, abnormal ECG (typical SQT changes), radionuclide lung ventilation, perfusion scan and other changes have a greater significance for the diagnosis of pulmonary embolism, pulmonary angiography is more meaningful for the diagnosis of pulmonary embolism.

3. Severe pneumonia Severe pulmonary infections including bacterial pneumonia, viral pneumonia, miliary tuberculosis, etc. can cause ARDS, however, some patients with severe pneumonia (especially such as Legionella pneumonia) have difficulty breathing, hypoxemia and other similar ARDS clinical Performance, but did not occur ARDS, most of them have large infiltrative inflammation shadows in the lung parenchyma, infection symptoms (fever, increased white blood cells, left shift of the nucleus), and the use of sensitive antibacterial drugs can be cured.

4. Idiopathic pulmonary fibrosis in some patients with idiopathic pulmonary fibrosis is subacute development, with type II respiratory failure, especially in the case of increased pulmonary infection, may be confused with ARDS, the chest auscultation of this disease Velcro voice, chest X-ray examination is reticular, nodular shadow or accompanied by cellular changes, the course of disease development is relatively slower than ARDS, lung function is limited ventilatory disorder can be identified.

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